ReviewApoptosis : an international journal on programmed cell death2025
Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.
Review in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
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Who cites it
6 citing papers in PubMed.
- CircRNA-regulated programmed cell death networks in cardiomyocytes: Molecular crosstalk and therapeutic translation.Non-coding RNA research · 2026Review
- ENPP2 Protects Mouse Myocardium from Ischemia-Reperfusion-Induced Ferroptosis Injury Via the SIRT1/PGC-1α/NRF1 Pathway.Applied biochemistry and biotechnology · 2026Article
- Lycopene's Role in Mitigating Obesity-Induced Cardiac Remodeling: Insights Into Inflammatory and MMP-2 Pathways.Molecular nutrition & food research · 2026Article
- Nanoparticle-Based Therapeutic Strategies for Pathological Cardiac Hypertrophy: Preclinical Advances, Translational Challenges, and Future Perspectives.International journal of nanomedicine · 2026Review
- Mechanistic study of Shenge powder on myocardial hypertrophy and cardiac lymphatic intervention in TAC-induced mouse models.Frontiers in pharmacology · 2026Article
- Decoding cardiac metabolic reprogramming through single-cell multi-omics: from mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Pressure overload hypertrophic cardiomyopathy (PO-HCM), a prevalent cardiovascular condition, is characterized by the heart's adaptive response to chronic pressure overload. However, excessive pressure overload contributes to cardiomyocyte dysfunction and pathological hypertrophy. The pathological hallmarks of PO-HCM include the abnormal enlargement of cardiomyocytes (hypertrophy) and structural remodeling of myocardial tissue. The pathogenesis is multifaceted and involves hemodynamic alterations, imbalances in neurohumoral regulation, and intracellular signaling pathway abnormalities. Within this pathological context, programmed cell death is critically involved in cardiomyocytes. This review synthesizes current research on programmed cell death mechanisms in PO-HCM-including apoptosis, necroptosis, pyroptosis, autophagy, and ferroptosis-to inform translational research and guide future therapeutic development.
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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.