Aging-US

In the fourth episode of the Longevity & Aging Series, Dr. Carly Bobak from Dartmouth College, Dr. Cristian Coarfa from Baylor College of Medicine, and Dr. Andrew DiNardo from Baylor College of Medicine, discuss a research paper they co-authored that was published in Volume 14, Issue 5, of Aging (Aging-US), entitled, “Increased DNA methylation, cellular senescence and premature epigenetic aging in guinea pigs and humans with tuberculosis.” DOI - https://doi.org/10.18632/aging.203936 Corresponding Authors - Carly A. Bobak - carlybobak@dartmouth.edu, Cristian Coarfa - coarfa@bcm.edu, and Andrew R. DiNardo - andrew.dinardo@bcm.edu Abstract Background: Tuberculosis (TB) is the archetypical chronic infection, with patients having months of symptoms before diagnosis. In the two years after successful therapy, survivors of TB have a three-fold increased risk of death. Methods: Guinea pigs were infected with Mycobacterium tuberculosis (Mtb) for 45 days, followed by RRBS DNA methylation analysis. In humans, network analysis of differentially expressed genes across three TB cohorts were visualized at the pathway-level. Serum levels of inflammation were measured by ELISA. Horvath (DNA methylation) and RNA-seq biological clocks were used to investigate shifts in chronological age among humans with TB. Results: Guinea pigs with TB demonstrated DNA hypermethylation and showed system-level similarity to humans with TB (p-value = 0.002). The transcriptome in TB in multiple cohorts was enriched for DNA methylation and cellular senescence. Senescence associated proteins CXCL9, CXCL10, and TNF were elevated in TB patients compared to healthy controls. Humans with TB demonstrate 12.7 years (95% CI: 7.5, 21.9) and 14.38 years (95% CI: 10.23–18.53) of cellular aging as measured by epigenetic and gene expression based cellular clocks, respectively. Conclusions: In both guinea pigs and humans, TB perturbs epigenetic processes, promoting premature cellular aging and inflammation, a plausible means to explain the long-term detrimental health outcomes after TB. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.203936 Longevity & Aging Series Aging (Aging-US) and FOXO Technologies have teamed up for a special collaboration on aging research with a monthly video series: Longevity & Aging Series. This series invites Aging researchers to speak with host Dr. Brian Chen, an adjunct faculty member at the University of California San Diego and Chief Science Officer of FOXO Technologies. Learn more - https://www.aging-us.com/longevity Keywords - aging, tuberculosis, multi-cohort analysis, network analysis, DNA methylation, senescence, Cavia porcellus, DNA hypermethylation, epigenetic aging About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published in Aging (“Aging (Albany NY)” by Medline/PubMed, “Aging-US” by Web of Science) Volume 14, Issue 16, entitled, “Systemic lipolysis promotes physiological fitness in Drosophila melanogaster.” A large body of literature shows that lipid metabolism exerts profound regulatory effects on aging and affects stress responses. Interventions such as caloric restriction or fasting robustly promote lipid catabolism and improve aging-related phenotypical markers. Researchers Linshan Shang, Elizabeth Aughey, Huiseon Kim, Timothy D. Heden, Lu Wang, Charles P. Najt, Nicholas Esch, Sophia Brunko, Juan E. Abrahante, Marissa Macchietto, Mara T. Mashek, Todd Fairbanks, Daniel E. L. Promislow, Thomas P. Neufeld, and Douglas G. Mashek from the University of Minnesota and University of Washington investigated the direct effect of increased lipid catabolism via overexpression of bmm (brummer, FBgn0036449), the major triglyceride hydrolase in Drosophila, on lifespan and physiological fitness. Comprehensive characterization was carried out using RNA-seq, lipidomics and metabolomics analysis. Global overexpression of bmm strongly promoted numerous markers of physiological fitness, including increased female fecundity, fertility maintenance, preserved locomotion activity, increased mitochondrial biogenesis and oxidative metabolism. Since bmm drives fatty acid oxidation, the data in this study implicated differential partitioning of glucose into the pentose phosphate pathway and purine biosynthesis between males and females. However, the underlying mechanisms through which bmm elicits these sex-specific effects remains to be determined. “Increased bmm robustly upregulated the heat shock protein 70 (Hsp70) family of proteins, which equipped the flies with higher resistance to heat, cold, and ER [endoplasmic reticulum] stress via improved proteostasis.” Despite improved physiological fitness, bmm overexpression did not extend lifespan. Taken together, these data show that bmm overexpression has broad beneficial effects on physiological fitness, but not lifespan. “Collectively, these studies reveal diverse beneficial effects of global elevation of lipolysis on physiological fitness. This work provides additional rationale for pursuing therapeutic approaches, as done previously [39], that enhance lipolysis to mitigate metabolic and aging-related diseases.” DOI: https://doi.org/10.18632/aging.204251 Corresponding Author: Douglas G. Mashek – Email: dmashek@umn.edu Keywords: brummer, lipolysis, physiological fitness, stress resistance, proteostasis Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204251 About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com​​ and connect with us: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Reddit – https://www.reddit.com/user/AgingUS Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com

A new research paper was published in Aging (“Aging (Albany NY)” by Medline/PubMed, “Aging-US” by Web of Science) on the cover of Volume 14, Issue 16, entitled, “Synergism of BCL-2 family inhibitors facilitates selective elimination of senescent cells.” Cellular senescence, a complex cellular response to stress characterized by a halt of cell cycle progression, is one factor contributing to aging. Accumulation of senescent cells in tissues with advancing age participates in the pathogenesis of several human age-associated diseases. Specific senescent secretome, the resistance of senescent cells to apoptotic stimuli, and lack of immune system response contribute to the accumulation of senescent cells and their adverse effects in tissues. Inhibition of antiapoptotic machinery, augmented in senescent cells, by BCL-2 protein family inhibitors represents a promising approach to eliminate senescent cells from tissues. “In this study, with the goal of decreasing the toxicity and potential onset of resistance to senolytic BCL-2 inhibitor monotherapy, we explored the effects of combined treatment covering both BCL-2 and MCL-1 anti-apoptotic factors in human cells.” Researchers David Rysanek, Pavla Vasicova, Jayaprakash Narayana Kolla, David Sedlak, Ladislav Andera, Jiri Bartek, and Zdenek Hodny from the Czech Academy of Sciences and the Danish Cancer Society Research Center aimed to explore synergistic and selective senolytic effects of anti-apoptotic BCL-2 family targeting compounds, particularly BH3 mimetics. “Using human non-transformed cells RPE-1, BJ, and MRC-5 brought to ionizing radiation-, oncogene-, drug-induced and replicative senescence, we found synergy in combining MCL-1 selective inhibitors with other BH3 mimetics.” In an attempt to uncover the mechanism of such synergy, the team revealed that the surviving subpopulation of cells resistant to individually applied ABT-737/ABT-263, MIK665, ABT-199, and S63845 BCL-2 family inhibitors showed elevated MCL-1 compared to untreated control cells indicating the presence of a subset of cells expressing high MCL-1 levels and, therefore, resistant to BCL-2 inhibitors within the original population of senescent cells. Overall, the researchers found that combining BCL-2 inhibitors can be beneficial for eliminating senescent cells, thereby enabling use of lower, potentially less toxic, doses of drugs compared to monotherapy, thereby overcoming the resistance of the subpopulation of senescent cells to monotherapy. DOI: https://doi.org/10.18632/aging.204207 Corresponding Author: Jiri Bartek, Zdenek Hodny – Email: jb@cancer.dk, hodny@img.cas.cz Keywords: homoharringtonine, cellular senescence, BCL-2, MCL-1, senolytics Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204207 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/

Listen to a blog summary of a trending research paper published by Aging, entitled, "Regulation of microglial activation in stroke in aged mice: a translational study.“ __________________________________________ A stroke can occur when the blood supply in and around the brain becomes interrupted. A hemorrhagic stroke is when a blood vessel bursts in or near the brain. An ischemic stroke is caused when a blood vessel carrying oxygen and nutrients to the brain is obstructed—usually by a clot. The most common type of stroke is ischemic, which accounts for approximately 87% of all strokes in humans. A major risk factor for an ischemic stroke is aging. Inflammation (a chronic condition among the elderly) is a key contributing factor to strokes, and microglia are the primary immune cells in the brain. Researchers recently identified a role for the microglial IRF5-IRF4 regulatory axis in mediating responses after stroke. However, whether or not aged microglia also undergo the same regulatory mechanisms after a stroke had previously not been determined. “Microglial activation plays a central role in initiating and perpetuating the post-stroke inflammation, and acts as a ‘double-edged’ sword to confer both detrimental and beneficial effects [9].” In a recent study, researchers Conelius Ngwa, Abdullah Al Mamun, Shaohua Qi, Romana Sharmeen, Yan Xu, and Fudong Liu from The University of Texas Health Science Center at Houston investigated aged mice and the role of the microglial IRF5-IRF4 regulatory axis after a stroke. On August 12, 2022, their research paper was published in Aging’s Volume 14, Issue 15, and entitled, “Regulation of microglial activation in stroke in aged mice: a translational study.“ Full blog - https://aging-us.org/2022/08/stroke-outcomes-mediated-by-these-2-mechanisms/ DOI - https://doi.org/10.18632/aging.204216 Corresponding author - Fudong Liu - Fudong.Liu@uth.tmc.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204216 Keywords - aging, inflammation, IRF, inflammation, microglia, stroke About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

In the third episode of the Longevity & Aging Series, Dr. Steve Horvath, Professor of Human Genetics and Biostatistics at UCLA, and Principal Investigator at Altos Labs, discusses the evolution of aging research and epigenetic clocks with host Brian Chen. Special Collection on Steve Horvath's Publications in Aging - https://www.aging-us.com/special-collections-archive/steve-horvath Author contact - Steve Horvath - shorvath@mednet.ucla.edu Longevity & Aging Series - https://www.aging-us.com/longevity Transcript - https://aging-us.net/2022/08/23/longevity-aging-series-ep-3-dr-steve-horvath-epigenetic-clocks/ About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com​​ or connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Listen to a blog summary of a trending research paper featured as the cover for Volume 14, Issue 15 of Aging (Aging-US), entitled, "Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival." _____________________________ Successful, or healthy, aging may be the result of adherence to several protective factors simultaneously within all three of the well-being domains. Previously, the majority of research on healthy aging has been limited to a single domain per study. In a new study, researchers Marguerita Saadeh, Xiaonan Hu, Serhiy Dekhtyar, Anna-Karin Welmer, Davide L. Vetrano, Weili Xu, Laura Fratiglioni, and Amaia Calderón-Larrañaga (from Karolinska Institutet, Karolinska University Hospital, Stockholm University, Lund University, and Stockholm Gerontology Research Center) believe that the vast heterogeneity in aging phenotypes cannot be explained by one domain of well-being alone. On July 18, 2022, their research paper was published on the cover of Aging’s Volume 14, Issue 15, and entitled, “Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival.” Full blog - https://aging-us.org/2022/08/3-domains-of-well-being-extend-elderly-mobility-and-longevity/ DOI - https://doi.org/10.18632/aging.204182 Corresponding author - Marguerita Saadeh - marguerita.saadeh@ki.se Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204182 Keywords - aging, mobility, survival, well-being, older adults, successful aging About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Aging (Aging-US) Volume 14, Issue 15: https://www.aging-us.com/issue/v14i15 Research Paper (Cover): “Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival” https://doi.org/10.18632/aging.204182 Editorial: “Sex difference in epigenomic instability during human aging” https://doi.org/10.18632/aging.204199 Editorial: “NAD+ to assess health in aging humans” https://doi.org/10.18632/aging.204220 Editorial: “T cell senescence by N-glycan branching” https://doi.org/10.18632/aging.204239 Research Paper: “mtDNA variability determines spontaneous joint aging damage in a conplastic mouse model” https://doi.org/10.18632/aging.204153 Research Paper: “Senolytic drugs relieve pain by reducing peripheral nociceptive signaling without modifying joint tissue damage in spontaneous osteoarthritis” ​​https://doi.org/10.18632/aging.204204 Research Paper: “Ascorbic acid induces salivary gland function through TET2/acetylcholine receptor signaling in aging SAMP1/Klotho (-/-) mice” https://doi.org/10.18632/aging.204213 Research Paper: “Regulation of microglial activation in stroke in aged mice: a translational study” https://doi.org/10.18632/aging.204216 Research Paper: “PDCD10 promotes the aggressive behaviors of pituitary adenomas by up-regulating CXCR2 and activating downstream AKT/ERK signaling” https://doi.org/10.18632/aging.204206 Research Paper: “Influence of cardiovascular risk burden on pulmonary function trajectory: role of physical and social activities” https://doi.org/10.18632/aging.204201 Research Paper: “miRNA-338-3p inhibits the migration, invasion and proliferation of human lung adenocarcinoma cells by targeting MAP3K2” https://doi.org/10.18632/aging.204198 Research Paper: “Serial neurocognitive changes following transcatheter aortic valve replacement: comparison between low and intermediate-high risk groups” https://doi.org/10.18632/aging.204202 Research Paper: “MAB21L1 promotes survival of lens epithelial cells through control of αB-crystallin and ATR/CHK1/p53 pathway” https://doi.org/10.18632/aging.204203 Research Paper: “Interleukin-17D promotes lung cancer progression by inducing tumor-associated macrophage infiltration via the p38 MAPK signaling pathway” ​​https://doi.org/10.18632/aging.204208 Research Paper: “A signature constructed with mitophagy-related genes to predict the prognosis and therapy response for breast cancer” https://doi.org/10.18632/aging.204209 Research Paper: “Artemisia argyi exhibits anti-aging effects through decreasing the senescence in aging stem cells” https://doi.org/10.18632/aging.204210 Research Paper: “SIAH1-mediated RPS3 ubiquitination contributes to chemosensitivity in epithelial ovarian cancer” https://doi.org/10.18632/aging.204211 Research Paper: “CBXs-related prognostic gene signature correlates with immune microenvironment in gastric cancer” https://doi.org/10.18632/aging.204214 Research Paper: “Targeting circRNA-MAP4K2 for the treatment of diabetes-induced retinal vascular dysfunction” https://doi.org/10.18632/aging.204215 Research Paper: “The comprehensive expression and functional analysis of m6A modification “readers” in hepatocellular carcinoma” https://doi.org/10.18632/aging.204217 Research Paper: “Establishing and validating an ADCP-related prognostic signature in pancreatic ductal adenocarcinoma” https://doi.org/10.18632/aging.204221 Research Paper: “SAAL1, a novel oncogene, is associated with prognosis and immunotherapy in multiple types of cancer” https://doi.org/10.18632/aging.204224 Research Paper: “Comprehensive pan-cancer analysis reveals the prognostic value and immunological role of SPIB” https://doi.org/10.18632/aging.204225 Research Paper: “Clinical outcomes and potential therapies prediction of subgroups based on a ferroptosis-related long non-coding RNA signature for gastric cancer” https://doi.org/10.18632/aging.204227 Visit our website at https://www.Aging-US.com​​.

Listen to a blog summary of an editorial published in Volume 14, Issue 14 of Aging (Aging-US), entitled, "Restoring rhythm to prevent age-related fractures.” ________________________________ The circadian rhythm is a daily cycle (24 hours) of biological activity that is driven by an internal biological clock. A regular circadian rhythm is important for maintaining numerous facets of human life. Aging-related changes to this delicate rhythm have demonstrated negative consequences in many aspects of health, including bone health. “Among the many risk factors for osteoporosis, a new kid on the block is disruption of the biological clock.” On July 19, 2022, an editorial paper was published in Aging‘s Volume 14, Issue 14, entitled, “Restoring rhythm to prevent age-related fractures.” In this editorial, Annelies E. Smit, Maaike Schilperoort and Elizabeth M. Winter from Leiden University Medical Center discuss the treatment of osteoporosis by way of restoring the circadian rhythm. The researchers review the use of both medical and lifestyle interventions that aim to restore the circadian rhythm to minimize the risk of aging-related osteoporotic fractures. Full blog - https://aging-us.org/2022/08/osteoporosis-linked-to-age-related-changes-in-circadian-rhythm/ DOI - https://doi.org/10.18632/aging.204192 (PDF Download) Corresponding author - Elizabeth M. Winter - e.m.winter@lumc.nl Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204192 Keywords - aging, circadian rhythm, fractures, osteoporosis, glucocorticoids, chronotherapy About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published in Aging (Aging-US) Volume 14, Issue 14, entitled, “Common electrocardiogram measures are not associated with telomere length.” Aging is accompanied by telomere shortening. Increased telomere shortening is considered a marker of premature aging. Cardiac aging results in the development of cardiac pathologies. Electrocardiogram (ECG) measures reflect cardiac excitation, conduction, and repolarization. ECG measures also prolong with aging and are associated with cardiac pathologies including atrial fibrillation. As premature prolongation of ECG measures is observed, researchers (Aenne S. von Falkenhausen, Rebecca Freudling, Melanie Waldenberger, Christian Gieger, Annette Peters, Martina Müller-Nurasyid, Stefan Kääb, and Moritz F. Sinner), from Ludwig-Maximilians-University Munich, Partner Site Munich Heart Alliance, German Research Center for Environmental Health, and Johannes Gutenberg University, hypothesized that such prolongation may be associated with telomere length. “We studied the large, community-based KORA F4 Study. Of 3,080 participants enrolled between 2006 and 2007 with detailed information on demographic, anthropometric, clinical, and ECG characteristics, 2,575 presented with available data on leukocyte telomere length.” Telomere length was determined by real-time quantitative PCR and expressed relative to a single copy gene. The researchers fitted multivariable adjusted linear regression models to associate the ECG measures RR-interval, PR-interval, QRS-duration, and heart rate corrected QTc with telomere length. In this cohort, the mean age was 54.9±12.9 years and 46.6% were men. Increased age was associated with shorter telomere length (p<0.01), and men had shorter telomere length than women (p<0.05). In unadjusted models, heart rate (p=0.023), PR-interval (p<0.01), and QTc-interval (p<0.01) were significantly associated with shorter telomere length. However, no significant associations remained after accounting for age, sex, and covariates. The researchers found that ECG measures are age-dependent, but not associated with shortened telomere length as a marker of biological aging. Further research is warranted to clarify if shortened telomeres are associated with clinical cardiac pathologies including atrial fibrillation. “In conclusion, ECG measures are clearly age-dependent. However, in a large, well-characterized, and sufficiently powered cohort we were not able to substantiate the hypothesis that telomere length as a marker of biological age is a relevant contributor to this age-dependent prolongation of ECG measures.” DOI: https://doi.org/10.18632/aging.204149 Corresponding Author: Moritz F. Sinner – Email: moritz.sinner@med.uni-muenchen.de Keywords: electrocardiogram, telomere length, cardiac aging About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com​​ and connect with us: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Reddit – https://www.reddit.com/user/AgingUS Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com

In the second installment of the Longevity & Aging Series, Dr. Steve Horvath, a world-renowned researcher, geneticist, biostatistician, Professor of Human Genetics and Biostatistics at the University of California, and Principal Investigator at Altos Labs, revisits 29 papers he co-authored that were published by Aging (Aging-US) and featured as a special collection of his research. Special Collection - https://www.aging-us.com/special-collections-archive/steve-horvath Author contact - Steve Horvath - shorvath@mednet.ucla.edu About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ or connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM