ReviewClinical science (London, England : 1979)2011
Molecular mechanisms of cardiomyocyte aging.
Review in Clinical science (London, England : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Oxidative Stress and Cardiovascular Aging: Interaction Between NRF-2 and ADMA.Current cardiology reviews · 2017Pooled it
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Aging: Current Insights and Therapeutic Advances.Biomedicines · 2026Review
- Inducing Oxidative Stress-Driven Senescent Phenotype in Induced Pluripotent Stem Cell Derived Cardiomyocytes.Cell biochemistry and biophysics · 2025Article
- Viability and Longevity of Human Miniaturized Living Myocardial Slices.Journal of cardiovascular development and disease · 2025Article
- Age-Associated Perinexal Narrowing Masks Consequences of Sodium Channel Gain of Function in Guinea Pig Hearts.JACC. Clinical electrophysiology · 2025Article
- Chronic moderate‑intensity exercise can induce physiological hypertrophy in aged cardiomyocytes through autophagy, with minimal Yap/Taz involvement.Biomedical reports · 2025Article
- Immunometabolism in the Aging Heart.Journal of the American Heart Association · 2025Review
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- Morphology of human sinoatrial node and its surrounding right atrial muscle in the global obesity pandemic-does fat matter?Frontiers in medicine · 2024Article
- In need of age-appropriate cardiac models: Impact of cell age on extracellular matrix therapy outcomes.Aging cell · 2023Article
- Cardiac System during the Aging Process.Aging and disease · 2023Review
- An integral perspective of canonical cigarette and e-cigarette-related cardiovascular toxicity based on the adverse outcome pathway framework.Journal of advanced research · 2023Review
- Spatiotemporal changes of tissue glycans depending on localization in cardiac aging.Regenerative therapy · 2023Article
- Review
- Modelling premature cardiac aging with induced pluripotent stem cells from a hutchinson-gilford Progeria Syndrome patient.Frontiers in physiology · 2022Article
- Diagnostic and Therapeutic Roles of Extracellular Vesicles in Aging-Related Diseases.Oxidative medicine and cellular longevity · 2022Review
- Melatonin as an Anti-Aging Therapy for Age-Related Cardiovascular and Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
- Review
- Exercise, programmed cell death and exhaustion of cardiomyocyte proliferation in aging zebrafish.Disease models & mechanisms · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Western societies are rapidly aging, and cardiovascular diseases are the leading cause of death. In fact, age and cardiovascular diseases are positively correlated, and disease syndromes affecting the heart reach epidemic proportions in the very old. Genetic variations and molecular adaptations are the primary contributors to the onset of cardiovascular disease; however, molecular links between age and heart syndromes are complex and involve much more than the passage of time. Changes in CM (cardiomyocyte) structure and function occur with age and precede anatomical and functional changes in the heart. Concomitant with or preceding some of these cellular changes are alterations in gene expression often linked to signalling cascades that may lead to a loss of CMs or reduced function. An understanding of the intrinsic molecular mechanisms underlying these cascading events has been instrumental in forming our current understanding of how CMs adapt with age. In the present review, we describe the molecular mechanisms underlying CM aging and how these changes may contribute to the development of cardiovascular diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.