ArticleThe Journal of clinical investigation2003
A mechanistic role for cardiac myocyte apoptosis in heart failure.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 303 papers.
What it found
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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.
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Who cites it
303 citing papers in PubMed, 739 citations in OpenAlex.
- Mechanistic insights into the mitigating role of dapagliflozin against radiation-triggered myocardial apoptosis: gating to AMPK-regulated autophagic machinery.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Regulated cell death programs shaping cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- The atypical E3 ligase HOIL-1 safeguards the ribosome during cellular stress.Nature cell biology · 2026Article
- Infiltrative and Inflammatory Cardiomyopathies: Using Imaging to Probe Mechanisms of Myocardial Dysfunction.Journal of cardiac failure · 2026Review
- METTL14-dependent mbioRxiv : the preprint server for biology · 2026Article
- Short-term intermittent hypoxia induces biphasic apoptotic responses in the murine heart.Scientific reports · 2026Article
- BAK and BAX: Therapeutic Targets for Acute Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury.Biology · 2025Review
- Single-cell dynamics reveal a stress-induced decision between hypertrophy and apoptosis in neonatal rat cardiomyocytes.Journal of molecular and cellular cardiology plus · 2025Article
- One Syndrome, Many Faces: A Unified Perspective on Heart Failure Phenotypes.International journal of molecular sciences · 2025Review
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- Apoptosis in Cardiac Conditions Including Cirrhotic Cardiomyopathy.International journal of molecular sciences · 2025Review
- Caspases as master regulators of programmed cell death: apoptosis, pyroptosis and beyond.Experimental & molecular medicine · 2025Review
- Exosomal non-coding RNAs: key regulators of inflammation-related cardiovascular disorders.European journal of medical research · 2025Review
- Klotho in age-related cardiovascular diseases: Insights into mitochondrial dysfunction and cell death.International journal of cardiology. Heart & vasculature · 2025Review
- Enhanced FGF21 Delivery via Neutrophil-Membrane-Coated Nanoparticles Improves Therapeutic Efficacy for Myocardial Ischemia-Reperfusion Injury.Nanomaterials (Basel, Switzerland) · 2025Article
- Mitochondrial Dysfunction in Congenital Heart Disease.Journal of cardiovascular development and disease · 2025Review
- Regulatory mechanisms of mAmerican journal of translational research · 2025Review
- Exploring the Cardiovascular Protective Effects of Baicalin: A Pathway to New Therapeutic Insights.Current topics in medicinal chemistry · 2025Review
243 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Heart failure is a common, lethal condition whose pathogenesis is poorly understood. Recent studies have identified low levels of myocyte apoptosis (80-250 myocytes per 10(5) nuclei) in failing human hearts. It remains unclear, however, whether this cell death is a coincidental finding, a protective process, or a causal component in pathogenesis. Using transgenic mice that express a conditionally active caspase exclusively in the myocardium, we demonstrate that very low levels of myocyte apoptosis (23 myocytes per 10(5) nuclei, compared with 1.5 myocytes per 10(5) nuclei in controls) are sufficient to cause a lethal, dilated cardiomyopathy. Interestingly, these levels are four- to tenfold lower than those observed in failing human hearts. Conversely, inhibition of cardiac myocyte death in this murine model largely prevents the development of cardiac dilation and contractile dysfunction, the hallmarks of heart failure. To our knowledge, these data provide the first direct evidence that myocyte apoptosis may be a causal mechanism of heart failure, and they suggest that inhibition of this cell death process may constitute the basis for novel therapies.
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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.