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                    <title><![CDATA[Cedars-Sinai Newsroom | Health Breakthroughs & Expert News]]></title>
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                    <pubDate>Thu, 10 Sep 2026 17:01:23 +0200</pubDate>
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                        <title><![CDATA[Cedars-Sinai Newsroom | Health Breakthroughs & Expert News]]></title>
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                        <title>Blocking a Protein May Reduce Buildup of Harmful Aging Cells</title>
                        <link>https://www.cedars-sinai.org/newsroom/blocking-a-protein-may-reduce-buildup-of-harmful-aging-cells/</link>
                        <guid>https://www.cedars-sinai.org/newsroom/blocking-a-protein-may-reduce-buildup-of-harmful-aging-cells/</guid><pp:caseid>806135</pp:caseid><pp:subtitle>Cedars-Sinai Investigators Identify Possible Target for Therapies to Help Remove These Cells and Prevent Age-Related Health Problems</pp:subtitle><description><![CDATA[<p><span>A team led by </span><a href="https://www.cedars-sinai.edu/health-sciences-university.html"><span>Cedars-Sinai Health Sciences University</span></a><span> investigators has identified a protein that may hide aging cells from the body’s immune system, allowing them to build up and contribute to age-related health problems.</span></p><p><span><img class="image_resized image-style-align-right" style="width:215px;" src="https://content.presspage.com/uploads/2110/174f6614-8b00-4b9b-ae55-b2d24a083ade/800_selim-chaib-cedars-sinai.jpeg?x=1788473172786" alt="Selim Chaib, PhD" width="215" />The findings, published in </span><a href="https://www.cell.com/cell-metabolism/fulltext/S1550-4131(26)00339-6" target="_blank" rel="noreferrer noopener"><i><span>Cell Metabolism</span></i></a><span>, suggest that the protein, called PD-L2, could serve as a target for treatments designed to remove harmful aging cells or as a blood marker that helps researchers track them.</span></p><p><span>“Our findings suggest that PD-L2 may help aging cells stay in the body when they would normally be removed by the immune system,” said </span><a href="https://researchers.cedars-sinai.edu/Selim.Chaib"><span>Selim Chaib, PhD</span></a><span>, research assistant professor of Medicine at Cedars-Sinai and first and co-corresponding author of the study.</span></p><p><span>These harmful aging cells, called senescent cells, become damaged and stop dividing but do not die. The cells remain in tissues and release substances that promote inflammation and interfere with the function of nearby cells. Their buildup has been linked to age-related health problems.</span></p><p style="margin-left:0in;"><span>Investigators found that in laboratory mice, removing or blocking PD-L2 reduced the number of aging cells and levels of the inflammatory substances they produce. The mice were better able to process sugar and could grip objects with greater strength.</span></p><p style="margin-left:0in;"><span>Investigators also found that human aging cells produced more PD-L2 than younger cells, and levels of the protein increased in some human tissues with age.</span></p><p><span><img class="image_resized image-style-align-right" style="width:215px;" src="https://content.presspage.com/uploads/2110/be2550e3-9cd7-44a0-a943-7d19eeeede32/800_james-kirkland-md-cedars-sinai2.jpg?x=1788473198883" alt="James Kirkland, MD, PhD" width="215" />“If we can find a way to block this protein, we may be able to help the immune system get rid of these cells and potentially improve health problems linked with aging,” said </span><a href="https://researchers.cedars-sinai.edu/James.Kirkland?prevPageName=cs-org%3Acedars-sinai%3Anewsroom%3Acedars-sinai-experts-attend-world-health-expo-in-dubai"><span>James Kirkland, MD, PhD</span></a><span>, director of the Center for Advanced Gerotherapeutics and senior author of the study.</span></p><p><span>Future research will explore whether blocking PD-L2 can safely produce health benefits in human patients and help researchers better understand its role in age-related diseases.</span></p><p><i><span>Additional Cedars-Sinai authors include Larissa Langhi Prata, Masayoshi Suda, Andres Sola, Jia Nie, Hyungsoo Kim, Tamar Pirtskhalava, Nino Giorgadze, Nicolas Musi, Ze’ev Ronai, and Tamara Tchkonia.</span></i></p><p><i><span>Other authors include Thomas Mitchell, Zacharias Anastasiadis, Hawley Kunz, Stella Victorelli, Ricardo Lozano Flores, Moritz Weigl, Shimpei Kawamoto, Ken Uemura, Binsheng Wang, Christina Inman, Ailing Xue, Kurt Johnson, Jair Espindola-Netto, Sonja Suvakov, Jennet Hatamova, Erik Parker, Davyn Benitto Hartono, Vagisha Kulshreshtha, Jose Alberto Lopez-Dominguez, Aaron Deisinger, Allyson Palmer, Yi Zhu, Megan Weivoda, Anne Gingery, Robert Hromas, Vesna Garovic, João Passos, David Allison, Eiji Hara, Michael Jensen, Stefan Tullius, Manuel Serrano, Ming Xu, Ian Lanza, and Yuji Ikeno.</span></i></p><p><i><span>Funding: Work in the J.L.K. laboratory was supported by the US National Institutes of Health (NIH; grants R37AG013925, R33AG061456, and P01AG062413), the Connor Fund, Robert J. and Theresa W. Ryan, the Hevolution Foundation, and the Noaber Foundation. Y.I. was supported by the San Antonio Nathan Shock Center Pathology Core (NIH Grant P30AG13319), San Antonio Claude D. 445 Pepper Center (NIH P30 AG044271), and NIH grants R01AG070034 and R56AG057785. M.D.J.’s studies were supported by NIH grants DK-45343 and DK-40484. H.E.K. was supported by an NIH musculoskeletal research training grant (T32AR56950) and NIH grant K01DK134765. S.K. was supported by the Japan Science and Technology Agency (JST) JPMJFR2308 and Japan Society for the Promotion of Science (JSPS) JP23K06481. L.G.P.L.P was supported by NIH grant 1K01AG090692. The clinical trial (NCT03350906) was supported by grants UL1TR002377 from the National Center for Advancing Translational Sciences (NCATS) and NIH R01AG054454. Y.Z. was supported by the Hevolution Foundation. J.F.P. was supported by NIH grants R01AG068048, R01AG82708, and UG3CA268103 and the Glenn Foundation for Medical Research. S.V.G. is supported by a Robert and Arlene Kogod Center on Aging Career Development Award and a c-SiG Pilot and Feasibility Award. A.G. was supported by NIH grant R01AR076347. M.X. is supported by a Hevolution/AFAR New Investigator Award in Biology and Geroscience Research. This work was supported in part by NIH P30AG050886.</span></i></p><p><i><span>Disclosures: S.C. holds patents or pending patents on PD-L2 at Mayo Clinic and Spanish National Cancer Research Center, some of which had been licensed to Rejuveron Senescence Therapeutics. M.S. is a shareholder of Senolytic Therapeutics, Life Biosciences, Rejuveron Senescence Therapeutics, and Altos Labs. T.T., Y.Z., A.K.P., T.P., N.G., and J.L.K. have a financial interest related to this research, including patents and pending patents covering senolytic drugs and their uses that are held by Mayo Clinic.</span></i></p><p><span style="color:hsl(353,76%,49%);"><i><span><strong>Cedars-Sinai Health Sciences University is advancing groundbreaking research and educating future leaders in medicine, biomedical sciences and allied health sciences. </strong></span></i></span><a href="https://www.cedars-sinai.edu/health-sciences-university.html?prevPageName=cs-org%3Acedars-sinai%3Anewsroom%3Aai-analyzes-surgical-technique-to-improve-prostate-cancer-care"><span style="color:hsl(353,76%,49%);"><i><span><strong>Learn more</strong></span></i></span></a><span style="color:hsl(353,76%,49%);"><i><span><strong> about the university.</strong></span></i></span></p>]]></description><category><![CDATA[Exclude,Research,Aging,Aging Research,james-kirkland-885945,Kelsie Sandoval]]></category>
            <pubDate>Thu, 10 Sep 2026 08:00:00 -0700</pubDate>
            <enclosure url="https://content.presspage.com/uploads/2110/74b6d770-7a80-47de-bf0e-fc65312739f8/500_aging-cells-cedars-sinai.jpg?10000" length="0" type="image/jpg" />
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                <pp:imageOriginal>https://content.presspage.com/uploads/2110/74b6d770-7a80-47de-bf0e-fc65312739f8/aging-cells-cedars-sinai.jpg?10000</pp:imageOriginal><pp:imageTitle><![CDATA[Cedars-Sinai researchers identified a protein that may help aging cells evade the immune system. Image by Getty.]]></pp:imageTitle><pp:imageDescription><![CDATA[Digital illustration of cells.]]></pp:imageDescription></item><item>
                        <title>Research Tip Sheet: Zombie Cells, GLP-1RAs, Heart Surgery and Breast Cancer</title>
                        <link>https://www.cedars-sinai.org/newsroom/research-tip-sheet-zombie-cells-glp-1ras-heart-surgery-and-breast-cancer/</link>
                        <guid>https://www.cedars-sinai.org/newsroom/research-tip-sheet-zombie-cells-glp-1ras-heart-surgery-and-breast-cancer/</guid><pp:caseid>735174</pp:caseid><pp:subtitle>The Latest Advances From Cedars-Sinai Investigators</pp:subtitle><description><![CDATA[<h2><span style="color:#dc1e34;"><span><strong><img class="image_resized image-style-align-left" style="aspect-ratio:335/auto;width:335px;" src="https://content.presspage.com/uploads/2110/a1fb897b-d37f-4c21-9963-b1167ea91fb8/800_zombie-cells-research-cedars-sinai.jpg?x=1770149196426" alt="" width="335" height="auto"></strong>Preclinical Study Targets ‘Zombie’ Cells</span></span></h2><p><span>Senolytics—a class of drugs that reduce chronic inflammation and tissue damage in aging cells—are shown to eliminate 30% to 70% of “zombie” cells in the body. These zombie cells, known as senescent cells, stop dividing and don’t die, ultimately contributing to a host of diseases of aging, including cancer.</span></p><p><span>A preclinical study from Cedars-Sinai, published in </span><a href="https://onlinelibrary.wiley.com/doi/10.1111/acel.70358" target="_blank"><i><span>Aging Cell</span></i></a><i><span>,</span></i><span> had three key findings:</span></p><ul style="list-style-type:disc;"><li data-list-item-id="e4edb4e0e180fbdc640e19644a29e1521"><span>Senolytic drugs purge the most harmful cells, leaving less-harmful senescent cells behind.</span></li><li data-list-item-id="ead5ffa1ac944fe74e02977b475badf82"><span>These remaining “senolytic-resistant” senescent cells can be activated into tissue-damaging senescent cells by infections and other factors in the environment of senescent cells.</span></li><li data-list-item-id="e0e56e5546db8921b68979d215acbc126"><span>A new class of drugs, “senosensitizers,” can enable senolytics to eliminate these lurking senolytic-resistant “ticking time bomb” cells.</span></li></ul><p><span>Investigators found that in laboratory mice treated with senolytic drugs, the remaining senescent cells were less inflammatory and damaging than the cells removed by the treatment. Researchers also found that these remaining senescent cells, when activated into tissue-damaging cells by an inflammatory environment, become more vulnerable to senolytics than those in a stable environment.</span></p><p><span>Based on their findings that infections can make senescent cells become susceptible to senolytics, study authors theorize that targeting senescent cells with newly developed senosensitizers—and then senolytics—might allow more senescent cells to be removed than when using senolytics alone. This could remove senolytic-resistant senescent cells and reduce the impact of infections in previously apparently healthy older people.</span></p><p><span>“This drug combination, which is still in the preclinical phase, has the potential to target senescent cancer cells that persist after radiation and chemotherapy and may later reemerge as more aggressive disease,” said </span><a href="https://researchers.cedars-sinai.edu/James.Kirkland?prevPageName=cs-org%3Acedars-sinai%3Anewsroom%3Acedars-sinai-launches-healthy-aging-clinic"><span>James Kirkland, MD, PhD</span></a><span>, director of the Center for Advanced Gerotherapeutics and senior author of the study.</span></p><p><i><span>Additional Cedars-Sinai authors include Masayoshi Suda, Tamar Tchkonia, Selim Chaib, Larissa Langhi Prata, Tamar Pirtskhalava and Nino Giorgadze.</span></i></p><p><i><span>Additional authors include Utkarsh Tripathi, Vagisha Kulshreshtha, Bryan T. Piatkowski, Allyson K. Palmer, Christina Inman, Nathan Gasek, Ming Xu, Kurt O. Johnson, Yi Zhu, Renuka Kandhaya-Pillai, Stefan G. Tullius, Saranya P. Wyles, Rambabu Majji, Hari Krishna Yalamanchili and David B. Allison.</span></i></p><p><i><span>Funding: This work was supported by NIH grants R37AG013925 (J.L.K., T.T.), R33AG061456 (J.L.K., T.T.), R01AG066679 (M.X.), R01AG076642 (M.X.), R01AG064165 (S.G.T.), R01AG087387 (Y.Z.), the Connor Fund (J.L.K., T.T.), Robert J. and Theresa W. Ryan (J.L.K., T.T.), HF-GRO-­23-­ 1199148-­ 3 (J.L.K.), HF-­ GRO-­ 23-­ 1199262-­ 27 (Y.Z., M.S.), the JSPS Grants-­ in-­ Aid for Scientific Research Fund for the Promotion of Joint International Research (Fostering Joint International Research) 23KK0295 (M.S.), the Yamada Science Foundation (M.S.), and USDA/ARS grant CRIS 3092-­ 51000-­ 065-­ 003S (H.K.Y.) and the Noaber Foundation (J.L.K.). U.T. was supported by an American Heart Association predoctoral fellowship (917775).</span></i></p><p style="margin-left:0in;">&nbsp;</p><h2><span><strong><img class="image_resized image-style-align-left" style="aspect-ratio:335/auto;width:335px;" src="https://content.presspage.com/uploads/2110/25b91cde-ff6a-4ae2-b762-52b768b3223d/800_chronic-cough-cedars-sinai.jpg?x=1770149227366" alt="" width="335" height="auto"></strong></span><span style="color:#dc1e34;"><span>Cedars-Sinai Study Links GLP-1RA Drugs to Risk of Chronic Cough</span></span></h2><p><span>Patients who take the widely used Type 2 diabetes and obesity medications known as glucagon-like peptide-1 receptor agonists (GLP-1RAs) appear to be at increased risk of developing chronic cough,&nbsp;according to a new multicenter study led by Cedars-Sinai and published in </span><a href="https://jamanetwork.com/journals/jamaotolaryngology/fullarticle/2842204" target="_blank"><i><span>JAMA Otolaryngology – Head & Neck Surgery</span></i></a><span>.</span></p><p><span>GLP-1RA medications, marketed under many brand names, work by stimulating insulin release from the pancreas, lowering blood sugar&nbsp;and slowing digestion. As a result, these drugs may help people with Type 2 diabetes manage their blood sugar and help people with obesity lose weight.</span></p><p><span>Investigators reviewed 10 years of electronic medical records with data on more than 2 million Type 2 diabetes patients at 70 healthcare organizations. They compared records of individuals prescribed a GLP-1RA drug with those who were prescribed a non-GLP-1RA drug to treat diabetes, and found that GLP-1RA use was associated with a significantly increased risk of new chronic cough.</span></p><p><span>“Further research is needed to confirm the existence, strength and mechanisms of the association between GLP-1RA drugs and chronic cough,” said </span><a href="https://researchers.cedars-sinai.edu/Anca.Barbu"><span>Anca Barbu, MD</span></a><span>, associate professor in the Jim and Eleanor Randall Department of Surgery and the study’s corresponding author. “However, our findings highlight the importance of physicians and care providers asking patients with new-onset chronic cough about possible GLP-1RA use, and for healthcare providers prescribing these medications to discuss chronic cough as a possible side effect.”</span></p><p><i><span>The other Cedars-Sinai author is Neelaysh Vukkadala, MD.</span></i></p><p><i><span>Additional authors include Tyler J. Gallagher, MD, MPH; Diego E. Razura, MD; Albert Li, BA;&nbsp;and Ian Kim, PhD.&nbsp;</span></i></p><p>&nbsp;</p><h2><span><strong><img class="image_resized image-style-align-left" style="aspect-ratio:335/auto;width:335px;" src="https://content.presspage.com/uploads/2110/cec4e39f-fb9d-4427-b63d-bec36d3d2ec1/800_heart-surgery-outcomes-cedars-sinai.jpg?x=1770149250559" alt="" width="335" height="auto"></strong></span><span style="color:#dc1e34;"><span>Bodily Fluid Changes Linked to Poor Heart Surgery Outcomes</span></span></h2><p><span>Patients who lose or gain a significant amount of fluid after certain elective heart surgeries are more likely to be readmitted to the ICU, stay longer in the hospital or die than patients whose fluid levels remain stable, according to a new study from Cedars-Sinai. The findings, published in </span><a href="https://journals.lww.com/anesthesia-analgesia/fulltext/9900/association_of_postoperative_cumulative_fluid.1537.aspx" target="_blank"><i><span>Anesthesia & Analgesia</span></i></a><span>, could help improve patient care.</span></p><p><span>Investigators reviewed data on 2,557 patients who underwent nonemergency coronary artery bypass grafts, valve surgeries or a combination of the two. They calculated each patient’s total fluid intake (including oral and intravenous fluids and blood products) and output (including urine, stool and surgical drains), based on measurements taken in the operating room and in the ICU after surgery.</span></p><p><span>“It remains unclear whether changes in cumulative fluid balances above 1.5 liters on the day of ICU discharge actually cause adverse outcomes or are just associated with them,” said senior author </span><a href="https://researchers.cedars-sinai.edu/Joseph.Ebinger"><span>Joseph Ebinger, MD, MS</span></a><span>, associate professor of Cardiology and director of the Coronary Intensive Care Unit and Clinical Analytics in the </span><a href="https://www.cedars-sinai.org/programs/heart.html"><span>Smidt Heart Institute</span></a><span> at Cedars-Sinai. “Further study is called for. In the meantime, our findings suggest that greater attention to such variations may help improve outcomes for cardiac surgery patients.”</span></p><p><i><span>Other Cedars-Sinai authors are Abirami Kumaresan, George Gill, Jesse Navarrette, Tao Shen, Milad Sharifpour, Dominic Emerson, Joanna Chikwe and Susan Cheng.</span></i></p><p><i><span>Funding: This study was supported in part by a grant from the International Anesthesia Research Society and NIH grant: K23-HL153888. The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.</span></i></p><p>&nbsp;</p><h2><span style="color:#dc1e34;"><span><img class="image_resized image-style-align-left" style="aspect-ratio:335/auto;width:335px;" src="https://content.presspage.com/uploads/2110/8247fde9-0e55-413f-b287-0c1b3acf3a45/800_breast-cancer-patient-cedars-sinai.jpg?x=1770333984378" alt="" width="335" height="auto">Different Immune Cell Types Correlate with Breast Cancer Survival</span></span></h2><p><span>The quantities of specific types of immune cells that appear in and around a breast cancer tumor are correlated with the prognosis for the patient, according to a new study led by Cedars-Sinai. The findings have implications for use of immunotherapy in this disease, the second leading cause of cancer deaths among women in the U.S.</span></p><p><span>The study was published in the peer-reviewed journal </span><a href="https://www.cell.com/iscience/fulltext/S2589-0042(26)00134-3" target="_blank"><i><span>iScience</span></i></a><span>.</span></p><p><span>Investigators analyzed images from 12,285 female breast cancers, including estrogen-positive breast cancer, the most common type, in which cancer cells have a protein that binds to the hormone estrogen; estrogen-negative breast cancer, in which the cells lack this protein, was also studied.</span></p><p><span>Using artificial intelligence (AI), investigators calculated the percentages of different types of immune cells within the tumors, in nearby connective tissue (known as stroma) and in total for both areas. They examined the relationship between these percentages and the likelihood that the patient would die from breast cancer over a certain period of time after diagnosis. Two types of immune cells, CD8+ and CD20+, were found to be associated with a better prognosis in estrogen-positive breast cancer patients, whereas another cell type, CD163+, was associated with a poorer prognosis. CD8+ and FOXP3+ immune cells were associated with a better prognosis in estrogen-negative breast cancer.</span></p><p><span>“Our findings suggest that the immune system is an important predictor of outcome in hormone-positive breast cancer,” said </span><a href="https://researchers.cedars-sinai.edu/Paul.Pharoah"><span>Paul Pharoah, MD, PhD</span></a><span>, professor of cancer epidemiology in the Department of Computational Biomedicine at Cedars-Sinai and the study’s senior and corresponding author. “They support including this subset of patients in clinical trials of immune modulators, which could lead to improved treatments for women with this common cancer.”</span></p><p><i><span>Other authors include: Aaron J. Bernstein PhD, Renske Keeman MSc, Amber Hurson PhD, Fiona M. Blows PhD, Manjeet K. Bolla MSc, Jodi L. Miller PhD, Roger L. Milne PhD, Hugo Horlings MD, PhD, Alexandra J. van den Broek PhD, Clara Bodelon PhD, James M. Hodge JD, MPH, Alpa V. Patel PhD, Lauren R. Teras PhD, Federico Canzian PhD, Rudolf Kaaks PhD, Hermann Brenner MD, Ben Schöttker PhD, Sabine Behrens PhD, Jenny Chang-Claude PhD, Tabea Maurer DiplPsych, Nadia Obi PhD, Fergus J. Couch PhD1, H. Raza Ali PhD, Carlos Caldas MD, Irene Andrulis PhD, Gord Glendon MSc, Anna Marie Mulligan MD, Wilma Mesker PhD, Agnes Jager MD, PhD, Annette Heemskerk-Gerritsen PhD, Peter Devilee PhD, Scott M. Lawrence PhD, Jolanta Lissowska PhD, Karun Mutreja PhD, Thomas Ahearn PhD, Stephen Chanock MD, Maire A. Duggan MD, Diana Eccles PhD, J. Louise Jones MB ChB, PhD, Will Tapper PhD, Antoinette Hollestelle PhD, Maartje Hooning PhD, John Martens PhD, Carolien H.M. van Deurzen MD, PhD, Angela Cox PhD3, Simon S. Cross MB BS, Mikael Hartman MD, PhD, Jingmei Li PhD, Thomas C. Putti MD, Ute Hamann PhD, Muhammad Rashid MB BS, PhD, Ania Jakubowska PhD, Nicki Camp PhD, Melissa H. Cessna MD, Amy Berrington de Gonzalez DPhil, Katarzyna Bialkowska PhD, Jacek Gronwald PhD, Jan Lubiński MD, PhD, Siddhartha Yadav MD, Pietro Lio PhD, Doug F. Easton PhD, Mustapha Abubakar MD, PhD, Montse Garcia-Closas MD, DrPH,&nbsp; and Marjanka K. Schmidt, PhD.</span></i></p><p><i><span>Acknowledgements: The authors thank the Histology and Genomics Cores at the Cancer Research UK Cambridge Institute for technical support, and all patients, researchers, clinicians, and administrative personnel who contributed to the studies taking part in BCAST.&nbsp; The CPSII study investigators acknowledge the contribution to this study from central cancer registries supported through the Centers for Disease Control and Prevention's National Program of Cancer Registries and cancer registries supported by the National Cancer Institute's Surveillance Epidemiology and End Results Program.</span></i></p><p><i><span>BCAC was supported by Cancer Research UK grant: PPRPGMNov20\100002 and by core funding from the NIHR Cambridge Biomedical Research Centre (NIHR203312). The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care.&nbsp; The BCAST project was supported by the Horizon 2020 Research and Innovation Programs of the European Union B (grant number: 633784) and the NIHR Cambridge Biomedical Research Centre. AJB was supported by the NIH Oxford-Cambridge Scholars and Gates Cambridge Scholars programs. (The funding of the contributing studies is listed in a supplementary table in the article.)</span></i></p><p><span style="color:#dc1e34;"><i><span><strong>Cedars-Sinai Health Sciences University is advancing groundbreaking research and educating future leaders in medicine, biomedical sciences and allied health sciences.&nbsp;</strong></span></i></span><a href="https://www.cedars-sinai.edu/health-sciences-university.html?adobe_mc=MCMID%3D79521921680015491943235909713257507329%7CMCORGID%3DF47CD0AC591352EC0A495E82%2540AdobeOrg%7CTS%3D1733161540"><span style="color:#dc1e34;"><i><span><strong>Learn more</strong></span></i></span></a><span style="color:#dc1e34;"><i><span><strong>&nbsp;about the university.</strong></span></i></span></p>]]></description><category><![CDATA[Exclude,Research,Newsroom Author,Kelsie Sandoval,Stephanie Cajigal,Jillian Scholten,Aging Research]]></category>
            <pubDate>Fri, 06 Feb 2026 06:00:00 -0800</pubDate>
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                <pp:image>https://content.presspage.com/uploads/2110/37635253-d1f0-4183-8440-87710bbb538b/500_graduate-research-education-cedars-sinai.jpg?10000</pp:image>
                <pp:imageOriginal>https://content.presspage.com/uploads/2110/37635253-d1f0-4183-8440-87710bbb538b/graduate-research-education-cedars-sinai.jpg?10000</pp:imageOriginal><pp:imageTitle><![CDATA[Joshua I. Goldhaber, MD, will oversee Cedars-Sinai&amp;rsquo;s PhD and master&amp;rsquo;s degree programs, postdoctoral research scientists, clinical scholars, physician-scientist training programs, and collaborative training and education with Cedars-Sinai&amp;rsquo;s affiliate universities. Photo by Cedars-Sinai.]]></pp:imageTitle><pp:imageDescription><![CDATA[A researcher in a lab.]]></pp:imageDescription></item><item>
                        <title>New Year’s Resolutions That Promote Healthy Aging</title>
                        <link>https://www.cedars-sinai.org/newsroom/new-years-resolutions-that-promote-healthy-aging/</link>
                        <guid>https://www.cedars-sinai.org/newsroom/new-years-resolutions-that-promote-healthy-aging/</guid><pp:caseid>732431</pp:caseid><pp:subtitle>Could Understanding the Long-Term Healthspan Benefits of New Year’s Resolutions Help You Keep Them?</pp:subtitle><description><![CDATA[<p><span>Following a joyful holiday season spent with loved ones, many people start the new year feeling sluggish—often from indulging in rich food and drinks or falling out of their workout routines.<img class="image_resized image-style-align-right" style="aspect-ratio:371/auto;width:371px;" src="https://content.presspage.com/uploads/2110/95d0d2c3-3cc8-4c57-80bd-4f5c343313ad/800_35385_med_geri_aging_diabetesamptranslationalgeroscienceleadership_sara_espinoza_md003.jpg?x=1767376717803" alt="Sara Espinoza, MD" width="371" height="auto"></span></p><p><span>Time for a change, said </span><a href="https://researchers.cedars-sinai.edu/Sara.Espinoza?adobe_mc=MCMID%3D03623767309869517462064686089986896399%7CMCORGID%3DF47CD0AC591352EC0A495E82%2540AdobeOrg%7CTS%3D1744649258&prevPageName=cs-org%3Acedars-sinai%3Anewsroom%3Acedars-sinai-launches-healthy-aging-clinic"><span>Sara Espinoza, MD</span></a><span>, medical director of the Cedars-Sinai Healthspan Clinic, which emphasizes maintaining a good quality of life while aging.&nbsp;</span></p><p><span>“If people are feeling guilty because they overindulged, my advice is, don’t wallow in it,” Espinoza said.&nbsp;“Every day is a new day, and it’s never too late to turn over a new leaf—especially in the new year.”</span></p><p><span>Although many earnestly make healthy resolutions, a </span><a href="https://www.forbes.com/health/mind/new-years-resolutions-statistics/" target="_blank"><span>2023 Forbes Health/OnePoll</span></a><span> showed that the average resolution lasts less than four months. Espinoza sat down with the </span><i><span>Cedars-Sinai Newsroom</span></i><span> to explain how resolving to practice healthy habits today—such as regular exercise and healthy eating—can affect long-term health. &nbsp;&nbsp;</span></p><h2><span><strong>For people who are not feeling their best after the holidays, what are some healthy resolutions they can make to start feeling better?</strong></span></h2><p><span>When people feel sluggish after the holidays, I usually start with recommending sleep. Sleep hygiene is critical for restoring energy, and one of the simplest steps is going to bed at the same time every night.</span></p><p><span>After sleep, consistent physical activity is one of the most effective ways to improve energy levels. If someone continues to feel fatigued despite improving sleep and exercise habits, that can be a signal of depression, and I recommend being screened.</span></p><h2><span><strong>What New Year's resolutions would you say have the biggest impact on longevity?</strong></span></h2><p><span>I almost always point to physical activity as having the greatest impact on long-term health.</span></p><p><span>I encourage people to aim for at least 150 minutes of cardiovascular exercise per week, along with resistance training two days a week. That resistance training does not have to be complicated and can include body-weight exercises.</span></p><p><span>If that amount of exercise feels out of reach, I don’t want people to get discouraged. Even starting with a resolution to walk more each day is beneficial, especially because there is evidence showing regular walking reduces the risk of heart disease and stroke.</span></p><p><span>My main message is any time working out is better than no time.</span></p><h2><span><strong>How do healthy daily habits support healthy aging and help prevent age-related diseases?</strong></span></h2><p><span>I talk frequently with patients about maintaining a healthy body weight because of its strong link to long-term health. Even modest weight loss—about 5% to 10% of body weight—can significantly reduce the risk of developing diabetes, sometimes by as much as 60%.</span></p><p><span>Research also shows that reducing calorie intake over several years can improve cardiovascular health, cholesterol levels and insulin sensitivity in young to middle-aged adults who are overweight or obese.</span></p><p><span>When discussing diet, I often reference </span><a href="https://nutritionsource.hsph.harvard.edu/healthy-eating-plate/" target="_blank"><span>Harvard’s Healthy Eating Plate</span></a><span>. About half the plate should be fruits and vegetables, a quarter should be whole grains such as brown rice or whole-wheat bread, and the remaining quarter should be healthy protein sources like fish, poultry, beans or nuts.</span></p><p><span>That said, dietary changes do not need to be extreme to be effective. If the guideline feels too strict, I suggest small, realistic adjustments, such as sharing a side of fries or choosing a salad instead.</span></p><p><span>People do not need to overhaul their entire diet overnight. Even one vegetable-focused meal a day as a resolution is a step in the right direction. Moderation is key.</span></p><h2><span><strong>Why is it so hard to stick to New Year’s resolutions, and what evidence-based strategies help people follow through?</strong></span></h2><p><span>One of the biggest reasons people struggle to stick with New Year’s resolutions is a lack of accountability. I often recommend working out with a friend, joining a class or having someone regularly check in.</span></p><p><span>Research on fitness trackers and wearables is mixed, but for many people, tracking progress is motivating. Simply monitoring daily steps on a phone or pedometer can help maintain consistency or reinforce habits.</span></p><p><span>I also encourage SMART goal setting, meaning goals that are specific, measurable, achievable, relevant and time bound. Starting with small, incremental steps is far more sustainable than setting unrealistic resolutions.</span></p><h2><span><strong>What are some underrated or often overlooked habits that can improve long-term health and aging?</strong></span></h2><p><span>One habit that often is overlooked is oral health. Poor dental health has been linked to cardiovascular disease and dementia.</span></p><p><span>To support oral health, I recommend brushing at least twice a day, flossing daily and limiting sugary foods and drinks. Again, if that is too rigid, even brushing teeth twice a day is a great resolution.</span></p><h2><span><strong>Are there any extra resolutions that promote healthy aging?</strong></span></h2><p><span>Although general guidelines are a helpful starting point, my medical recommendations to support healthy aging resolutions for the greatest impact are tailored to an individual’s health status.</span></p><p><span>For older adults, for example, weight loss requires careful consideration because it can lead to loss of both fat and muscle. In those cases, weight loss combined with resistance training can help preserve muscle mass and maintain strength.</span></p><p><span>For patients with cardiovascular disease, I often recommend not smoking, limiting alcohol, taking prescribed blood pressure medications and following a low-sodium diet.</span></p><p><span>To make an appointment with the Healthspan Clinic, call 310-423-3870 and select option 1 and ask to schedule an appointment with Espinoza.</span></p><p><span style="color:#dc1e34;"><i><span><strong>Read more from Cedars-Sinai Stories and Insights: </strong></span></i></span><a href="https://www.cedars-sinai.org/stories-and-insights/healthy-living/how-to-think-about-your-biological-age"><span style="color:#dc1e34;"><i><span><strong><u>How to Think About Your Biological Age</u></strong></span></i></span></a></p>]]></description><category><![CDATA[News,Aging,Healthy Aging,Kelsie Sandoval,Homepage,Aging Research]]></category>
            <pubDate>Tue, 13 Jan 2026 06:00:00 -0800</pubDate>
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                <pp:imageOriginal>https://content.presspage.com/uploads/2110/dfee5f95-19d2-4435-a1ad-3dfe38d5feb6/new-years-resolution-cedars-sinai.jpg?72895</pp:imageOriginal><pp:imageTitle><![CDATA[Sara Espinoza, MD, medical director of the Cedars-Sinai Healthspan Clinic, said moving more and eating more vegetables are New Year&amp;rsquo;s resolutions that support healthy aging. Image by Getty.]]></pp:imageTitle><pp:imageDescription><![CDATA[Note pad with text 2026 on wooden work desk. Planning resolutions for New Year 2026. Laptop, eyeglasses, pen.]]></pp:imageDescription></item><item>
                        <title>Aged Blood Vessel Cells Drive Metabolic Diseases</title>
                        <link>https://www.cedars-sinai.org/newsroom/aged-blood-vessel-cells-drive-metabolic-diseases/</link>
                        <guid>https://www.cedars-sinai.org/newsroom/aged-blood-vessel-cells-drive-metabolic-diseases/</guid><pp:caseid>729055</pp:caseid><pp:subtitle>Cedars-Sinai Preclinical Study Lays Foundation for Future Development of Treatments for Complex Diseases Like Diabetes</pp:subtitle><description><![CDATA[<p><span>Investigators from the Center for Advanced Gerotherapeutics at Cedars-Sinai found that aged blood vessel cells play a key role in the development of metabolic disorders, including diabetes. The preclinical findings, published in </span><a href="https://www.cell.com/cell-metabolism/fulltext/S1550-4131(25)00443-7" target="_blank"><i><span>Cell Metabolism</span></i></a><span>, could lead to new treatments for these complex disorders.</span></p><p><span>Obesity increases the accumulation of senescent cells, aged cells that have stopped dividing but have not died, in several organs and tissues.</span></p><p><span><img class="image_resized image-style-align-right" style="width:200px;" src="https://content.presspage.com/uploads/2110/9714c002-8989-42c5-a42f-d8e22ae35a24/500_masayoshi.suda.jpg?x=1763567538703" alt="Masayoshi Suda, MD, PhD" width="200">“Senescent cells differ depending on the originating cell types, diseases and other factors. Some senescent cells help with wound healing, but others cause harm and are known contributors to age-related diseases,” said </span><a href="https://researchers.cedars-sinai.edu/Masayoshi.Suda"><span>Masayoshi Suda, MD, PhD</span></a><span>, assistant professor of Medicine at Cedars-Sinai and lead author of the study. “Our goal is to identify and target these harmful types of senescent cells while sparing helpful cells.”</span></p><p><span>Previous research by the investigators showed that eliminating senescent cells with drugs called senolytics improved metabolic function, the body’s method for turning food and drink into energy.</span></p><p><span>In the current study, investigators focused on senescent blood vessel cells. They selectively removed these cells from obese laboratory mice and found that the animals’ inflammation and fat mass were reduced—and blood sugar levels improved.</span></p><p><span>When the investigators transplanted senescent blood vessel cells into lean laboratory mice, those mice developed inflammation in fat tissue and metabolic dysfunction.</span></p><p><span><img class="image_resized image-style-align-right" style="width:200px;" src="https://content.presspage.com/uploads/2110/be2550e3-9cd7-44a0-a943-7d19eeeede32/500_james-kirkland-md-cedars-sinai2.jpg?x=1763567774491" alt="James Kirkland, MD, PhD" width="200">Suda said this occurred because senescent blood vessel cells release high levels of inflammatory molecules.</span></p><p><span>The investigators next treated both groups of mice with fisetin, a naturally occurring senolytic compound, and found that the mice had fewer senescent blood vessel cells and improved diabetic symptoms. Investigators saw a similar decline in senescent blood vessel cells when they treated tissue samples from obese human patients with fisetin.</span></p><p><span>“Preliminary findings like these are crucial to translating aging research into clinical care,” said </span><a href="https://researchers.cedars-sinai.edu/James.Kirkland?prevPageName=cs-org%3Acedars-sinai%3Anewsroom%3Acedars-sinai-launches-healthy-aging-clinic"><span>James Kirkland, MD, PhD</span></a><span>, director of the Center for Advanced Gerotherapeutics and senior author of the study. “While more research is needed, we aim to eventually treat multiple age-related diseases simultaneously by using fisetin and related senolytics for aging and metabolic health.”</span></p><p><span>Suda said his team will next work to test this approach in clinical trials.</span></p><p><span>“If we can target senescent cells safely in humans, it could help address not just diabetes but a range of age-related conditions,” he said.</span></p><p><i><span>Additional Cedars-Sinai authors include&nbsp;Selim Chaib, Larissa Langhi Prata, Tamar Pirtskhalava, Nino Giorgadze, Sara Espinoza, Nicolas Musi, and Tamar Tchkonia.</span></i></p><p><i><span>Additional authors include&nbsp;Yi Zhu, Utkarsh Tripathi, Karl Paul, Allyson Palmer, Vagisha Kulshreshtha, Christina Inman, Kurt Johnson, Runqing Huang, Carolyn Roos, Luisa Leon-Sanchez, Jordan Miller, Thomas White, Linshan Laux, Laura Niedernhofer, Paul Robbins, Sundeep Khosla and Stefan G. Tullius.</span></i></p><p><i><span>Disclosures:&nbsp;Tamar Tchkonia, Allyson Palmer, Yi Zhu and James L. Kirkland have a financial interest related to this research, including patents and pending patents covering senolytic drugs and their uses held by Mayo Clinic.</span></i></p><p><i><span>Funding: This work was supported by the US National Institutes of Health (NIH) grants R37AG013925, R33AG061456, P01AG062413 (J.L.K., S.K., L.J.N., P.D.R.), U54 AG079754 (P.D.R., S.K., L.J.N), P01AG43376 (P.D.R., L.J.N.), R01AG086085 (S.K.), R01AG087387 (Y.Z.), and R01 AG063543 (L.J.N.).&nbsp;</span></i></p><p><span style="color:#dc1e34;"><i><span style="text-align:left;"><strong>Cedars-Sinai Health Sciences University is advancing groundbreaking research and educating future leaders in medicine, biomedical sciences and allied health sciences.&nbsp;</strong></span></i></span><a href="https://www.cedars-sinai.edu/health-sciences-university.html"><span style="color:#dc1e34;"><i><span><strong>Learn more</strong></span></i></span></a><span style="color:#dc1e34;"><i><span style="text-align:left;"><strong>&nbsp;about the university.</strong></span></i></span></p>]]></description><category><![CDATA[Research,Exclude,Kelsie Sandoval,Newsroom Author,Aging,Geriatrics,Aging Research,Endocrinology Research]]></category>
            <pubDate>Thu, 20 Nov 2025 08:00:00 -0800</pubDate>
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                <pp:imageOriginal>https://content.presspage.com/uploads/2110/631da540-fd61-47c0-8b1e-78562e4db77a/human-cells-cedars-sinai.jpg?10000</pp:imageOriginal><pp:imageTitle><![CDATA[A preclinical study led by Cedars-Sinai found that removing senescent blood vessel cells improves metabolic function. Image by Getty.]]></pp:imageTitle><pp:imageDescription><![CDATA[Close-up illustration of biological cells.]]></pp:imageDescription></item><item>
                        <title>Cedars-Sinai, UCLA and USC Join Forces to Extend Human Healthspan</title>
                        <link>https://www.cedars-sinai.org/newsroom/cedars-sinai-ucla-and-usc-join-forces-to-extend-human-healthspan/</link>
                        <guid>https://www.cedars-sinai.org/newsroom/cedars-sinai-ucla-and-usc-join-forces-to-extend-human-healthspan/</guid><pp:caseid>725068</pp:caseid><pp:subtitle>A $6.5M NIH Grant to Cedars-Sinai, UCLA and USC will Help Expand the Number of Aging-Focused Clinical Trials With Goal of Improving Quality of Life for Older Adults</pp:subtitle><description><![CDATA[<p><span>Cedars-Sinai, UCLA and the University of Southern California have been awarded $6.5 million from the National Institutes of Health and the National Institute on Aging to establish a Claude D.&nbsp;Pepper Older Americans Independence&nbsp;Center in Los Angeles. The center will be part of a national consortium of 15 research institutions conducting clinical trials on aging, with the overall goal of improving quality of life for older adults.</span></p><p><span>Investigators at the Los Angeles Pepper Center will focus on extending older adults’ healthspan—which means aging with reduced burden of chronic diseases and conditions that lead to loss of independence—by studying interventions that target the biological processes of aging. Investigators then will translate those findings into clinical care.</span></p><p><span><img class="image_resized image-style-align-right" style="aspect-ratio:356/auto;width:356px;" src="https://content.presspage.com/uploads/2110/95d0d2c3-3cc8-4c57-80bd-4f5c343313ad/800_35385_med_geri_aging_diabetesamptranslationalgeroscienceleadership_sara_espinoza_md003.jpg?x=1760396835117" alt="Sara Espinoza, MD" width="356" height="auto">“This prestigious grant provides Cedars-Sinai the opportunity to expand its geroscience research within our institution, across Los Angeles, and beyond, with the long-term goal of offering evidence-based healthy aging guidance for older adults,” said </span><a href="https://www.cedars-sinai.org/provider/sara-espinoza-543828.html"><span>Sara Espinoza, MD</span></a><span>, director of the Cedars-Sinai Center for Translational Geroscience.</span></p><p><span>For the next five years, Espinoza will lead the Los Angeles Pepper Center in collaboration with colleagues at USC and UCLA who say the combined expertise and resources of the three prominent institutions is a strong advantage.</span></p><p><span>“This partnership allows us to accelerate breakthroughs that can directly improve quality of life for older adults,” said Pinchas Cohen, MD, dean of the USC Leonard Davis School of Gerontology and co-director of the new center.</span></p><p><span>The </span><a href="https://www.cdc.gov/cdi/indicator-definitions/older-adults.html" target="_blank"><span>Centers for Disease Control and Prevention</span></a><span> projects that nearly one-quarter of the U.S. population will be 65 or older by 2060. Researchers say this creates a critical need to address the onset of multiple chronic diseases linked to aging. By intervening in the aging process at the biological level, scientists aim to prevent, delay and treat multiple medical conditions simultaneously.</span></p><p><span>“This designation strengthens our commitment to addressing the health challenges of aging—not only for today’s older adults, but for future generations as well,” said Jonathan Wanagat, MD, PHD, a geriatrician at UCLA and co-director of the Pepper Center.</span></p><p><span>The Claude D. Pepper Older Americans Independence Center in Los Angeles has four aims: to further develop gerotherapeutics—drugs that target the underlying cellular aging processes—and increase the number of researchers, expand clinical trials, and share the latest findings in translational geroscience.</span></p><p><span>“The robust resources, network and infrastructure made possible by the NIH solidifies Los Angeles’ leading position in aging research and geriatric clinical care,” Espinoza said.&nbsp;</span></p><p><span style="color:#dc1e34;"><i><span style="text-align:left;"><strong>Read more in Cedars-Sinai&nbsp;</strong></span><strong>Discoveries</strong><span style="text-align:left;"><strong>&nbsp;Magazine: </strong></span></i></span><a href="https://www.cedars-sinai.org/discoveries/the-future-of-aging-research.html" target="_blank"><span style="color:#dc1e34;"><i><span style="text-align:left;"><strong>The Future of Aging Research</strong></span></i></span></a></p>]]></description><category><![CDATA[News,Aging,Healthy Aging,Research,sara-espinoza-543828,Kelsie Sandoval,Aging Research]]></category>
            <pubDate>Thu, 16 Oct 2025 08:00:00 -0700</pubDate>
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                <pp:imageOriginal>https://content.presspage.com/uploads/2110/e92dff4d-ae1e-4942-83b6-1d61f04f2ff2/picmpis.jpg?10000</pp:imageOriginal><pp:imageTitle><![CDATA[From left to right, Pinchas Cohen, MD, of USC, Sara Espinoza, MD, of Cedars-Sinai, and Jonathan Wanagat, MD, PhD, of UCLA, will lead a multicenter initiative to expand aging-focused clinical trials and advance healthy aging research. Photo by Cedars-Sinai.]]></pp:imageTitle><pp:imageDescription><![CDATA[A female physician-scientist, Sara Espinoza, MD, stands between two male physician-scientists,  Pinchas Cohen, MD, and Jonathan Wanagat, MD, PhD.]]></pp:imageDescription></item></channel>
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