ArticleJournal of the American Heart Association2017
Cardiomyocyte-Specific Telomere Shortening is a Distinct Signature of Heart Failure in Humans.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
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Who cites it
67 citing papers in PubMed, 106 citations in OpenAlex.
- Leukocyte telomere length and risk of heart failure with preserved ejection fraction in high-risk Chinese patients with hypertension under 65 years.GeroScience · 2026Observational
- Essential Role for Telomeric Repeat-Binding Factor 2 in Cardiac Development and Function.FASEB bioAdvances · 2026Article
- Senescence modulated cardiac repair with pluripotent stem cell-derived cardiomyocytes.Stem cell research & therapy · 2026Article
- Inflammation, metabolism, and aging in heart failure with preserved ejection fraction: Mechanisms and treatment perspectives.Journal of translational internal medicine · 2026Article
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Article
- Integrative transcriptomic profiling links telomere dysfunction to cGAS-STING activation in heart failure signatures in mice and humans.Cardiovascular research · 2026Article
- DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026Review
- The Biological Mechanisms of Frailty: Focusing on Cellular Senescence.European cardiology · 2026Review
- Cellular senescence and cell therapy in cardiovascular diseases.Stem cell research & therapy · 2025Review
- Associations of Midlife Leukocyte Telomere Length With Measures of Left Atrial Function in Community-Dwelling Older Adults: The ARIC Study.Journal of the American Heart Association · 2025Observational
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- Cellular senescence in age-related cardiovascular disease: past and future.Frontiers in aging · 2025Review
- Telomere length as a biomarker for cerebrovascular diseases: current evidence.Molecular biology reports · 2024Review
- NRF2 signaling pathway and telomere length in aging and age-related diseases.Molecular and cellular biochemistry · 2024Review
- Proximal telomeric decompaction due to telomere shortening drives FOXC1-dependent myocardial senescence.Nucleic acids research · 2024Article
- Associations of measured and genetically predicted leukocyte telomere length with vascular phenotypes: a population-based study.GeroScience · 2024Article
- The role of CYP-sEH derived lipid mediators in regulating mitochondrial biology and cellular senescence: implications for the aging heart.Frontiers in pharmacology · 2024Review
- Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024Article
- Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTelomere defects are thought to play a role in cardiomyopathies, but the specific cell type affected by the disease in human hearts is not yet identified. The aim of this study was to systematically evaluate the cell type specificity of telomere shortening in patients with heart failure in relation to their cardiac disease, age, and sex. METHODS AND
resultsWe studied cardiac tissues from patients with heart failure by utilizing telomere quantitative fluorescence in situ hybridization, a highly sensitive method with single-cell resolution. In this study, total of 63 human left ventricular samples, including 37 diseased and 26 nonfailing donor hearts, were stained for telomeres in combination with cardiomyocyte- or α-smooth muscle cell-specific markers, cardiac troponin T, and smooth muscle actin, respectively, and assessed for telomere length. Patients with heart failure demonstrate shorter cardiomyocyte telomeres compared with nonfailing donors, which is specific only to cardiomyocytes within diseased human hearts and is associated with cardiomyocyte DNA damage. Our data further reveal that hypertrophic hearts with reduced ejection fraction exhibit the shortest telomeres. In contrast to other reported cell types, no difference in cardiomyocyte telomere length is evident with age. However, under the disease state, telomere attrition manifests in both young and older patients with cardiac hypertrophy. Finally, we demonstrate that cardiomyocyte-telomere length is better sustained in women than men under diseased conditions.
conclusionsThis study provides the first evidence of cardiomyocyte-specific telomere shortening in heart failure.
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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.