ArticleThe EMBO journal2019
Length-independent telomere damage drives post-mitotic cardiomyocyte senescence.
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Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 305 papers.
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305citing papers in PubMed
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305 citing papers in PubMed, 496 citations in OpenAlex.
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Circular MIR144 from eccDNA is a superior senescence agonist in aging hearts.Signal transduction and targeted therapy · 2026Article
- Chronic Senolytic Treatment and/or Aerobic Exercise Reduce Senescence and Improve Myocardial Function During Aging in the Heart.Aging cell · 2026Article
- METTL14-Mediated mAging cell · 2026Article
- Post-mitotic cardiomyocyte senescence redefines cardiac ageing.Nature reviews. Cardiology · 2026Article
- Senescent Cell Heterogeneity: Tissue-Dependent Signatures and Age Dynamics Revealed by Human scRNA-Seq Data.International journal of molecular sciences · 2026Article
- Clearance of p16-positive cardiac cells improves age-related cardiac remodeling in mice.Experimental physiology · 2026Article
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- From aging biology to cardiac biotechnology: emerging platforms for modeling cardiac aging.JCI insight · 2026Review
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- The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.Trends in cardiovascular medicine · 2026Review
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- Isoproterenol Induces Cardiac Injury and Senescence in Sprague-Dawley Rats: A Cost-Effective Pharmacological Model.Biomedicines · 2026Article
- Senescence modulated cardiac repair with pluripotent stem cell-derived cardiomyocytes.Stem cell research & therapy · 2026Article
- Cellular Senescence and the SASP in HFpEF: Pathogenic Mechanisms and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Cellular senescence as a therapeutic target for aging intervention.Biomedical journal · 2026Review
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Inflammation, metabolism, and aging in heart failure with preserved ejection fraction: Mechanisms and treatment perspectives.Journal of translational internal medicine · 2026Article
- Inhibiting the Hif-1α-Drp1 axis alleviates mitochondrial dysfunction and reduces senescence-like changes in myocardial tissue after acute myocardial infarction.Biology direct · 2026Article
- Farnesyltransferase Deficiency in Cardiomyocytes Initiates Senescence and Contributes to Cardiac Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
245 more citing papers are in PubMed but not listed here.
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Authors and funding
34 authors at 8 institutions in 3 countries.
Rhys AndersonAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Anthony LagnadoAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Damien MaggioraniINSERM Institute of metabolic and cardiovascular diseases, University of Toulouse, Toulouse, France.ORCID 0000-0002-3647-7383
Anna WalaszczykCardiovascular Research Centre, Institute for Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Emily DookunInstitute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK.
James ChapmanAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Jodie BirchAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Hanna SalmonowiczAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Mikolaj OgrodnikAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Diana JurkAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Carole ProctorAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Clara Correia-MeloAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Stella VictorelliAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Edward FielderAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.
Rolando Berlinguer-PalminiThe Bio-Imaging Unit, Newcastle University, Newcastle upon Tyne, UK.ORCID 0000-0002-1786-496X
Andrew OwensCardiovascular Research Centre, Institute for Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Laura C GreavesWellcome Trust Centre for Mitochondrial Research, Centre for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, UK.
Kathy L KolskyRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA.
Angelo PariniINSERM Institute of metabolic and cardiovascular diseases, University of Toulouse, Toulouse, France.
Victorine Douin-EchinardINSERM Institute of metabolic and cardiovascular diseases, University of Toulouse, Toulouse, France.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA.
Helen M ArthurCardiovascular Research Centre, Institute for Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Simon Tual-ChalotCardiovascular Research Centre, Institute for Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
Marissa J SchaferRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA.
Carolyn M RoosRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA.
Jordan D MillerRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA.
Neil RobertsonInstitute of Cancer Sciences, CR-UK Beatson Institute, University of Glasgow, Glasgow, UK.
Jelena MannInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.
Peter D AdamsInstitute of Cancer Sciences, CR-UK Beatson Institute, University of Glasgow, Glasgow, UK.
Tamara TchkoniaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA.
James L KirklandRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA.
Jeanne Mialet-PerezINSERM Institute of metabolic and cardiovascular diseases, University of Toulouse, Toulouse, France Jeanne.Perez@inserm.fr Gavin.Richardson@ncl.ac.uk Passos.Joao@mayo.edu.ORCID 0000-0002-1765-0283
Gavin D RichardsonCardiovascular Research Centre, Institute for Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK Jeanne.Perez@inserm.fr Gavin.Richardson@ncl.ac.uk Passos.Joao@mayo.edu.ORCID 0000-0002-2310-9987
João F PassosAgeing Research Laboratories, Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK Jeanne.Perez@inserm.fr Gavin.Richardson@ncl.ac.uk Passos.Joao@mayo.edu.ORCID 0000-0001-8765-1890
Newcastle Hospitals - Campus for Ageing and Vitality · GBMayo Clinic in Florida · USCentre for Life · GBInserm · FRNewcastle University · GBCancer Research UK Scotland Institute · GBSanford Burnham Prebys Medical Discovery Institute · USWellcome Centre for Mitochondrial Research · GB
Funding
STRUCTURAL BASIS FOR EPIGENETICS IN AGING AND LONGEVITYP01AG031862 · NIA · WISTAR INSTITUTE · PI GARCIA, BENJAMIN A · 2008 to 2022
$28.3MEffect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6MEffect of Aging on Preadipocyte DifferentiationR01AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 1997 to 2012
$3.7MRole of senescent cells in the pathogenesis of Marfan-associated cardiovascular diseaseR01HL141819 · NHLBI · MAYO CLINIC ROCHESTER · PI MILLER, JORDAN D · 2018 to 2021
$1.6MBiotechnology and Biological Sciences Research Council BB/H022384/1British Heart Foundation PG/14/86/31177British Heart Foundation PG/15/85/31744British Heart Foundation PG/19/15/34269Medical Research Council G0700718Medical Research Council MR/L016354/1NHLBI NIH HHS R01 HL141819NIA NIH HHS P01 AG031862NIA NIH HHS R01 AG013925NIA NIH HHS R37 AG013925
Abstract
Ageing is the biggest risk factor for cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening, has been implicated in age-related tissue dysfunction. Here, we address the question of how senescence is induced in rarely dividing/post-mitotic cardiomyocytes and investigate whether clearance of senescent cells attenuates age-related cardiac dysfunction. During ageing, human and murine cardiomyocytes acquire a senescent-like phenotype characterised by persistent DNA damage at telomere regions that can be driven by mitochondrial dysfunction and crucially can occur independently of cell division and telomere length. Length-independent telomere damage in cardiomyocytes activates the classical senescence-inducing pathways, p21
Indexed as
Cellular SenescenceDNA DamageMitosisTelomere ShorteningAgingAnimalsCardiomegalyFemaleFibrosisHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMonoamine OxidaseMonoamine Oxidasemonoamine oxidase A, humanRNATelomerasetelomerase RNAageingcardiomyocytessenescencesenolyticstelomeres
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.