ReviewJournal of molecular and cellular cardiology2022
The role of autophagy in death of cardiomyocytes.
Review in Journal of molecular and cellular cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Bibliometric and visual analysis of doxorubicin-induced cardiotoxicity.Frontiers in pharmacology · 2023Pooled it
- RNF10 deficiency in cardiomyocytes impairs mitophagy and drives pathological hypertrophy.Acta pharmacologica Sinica · 2026Article
- Small-molecule autophagy modulators: Mechanisms, therapeutic potential, and development challenges in pathological settings.Fundamental research · 2026Review
- Crocetin Attenuates Fibroblast-to-Myofibroblast Transition after Myocardial Infarction in Mice by Regulating Autophagy.Cardiovascular drugs and therapy · 2026Article
- Peroxiredoxin Ⅲ safeguards cardiac function against doxorubicin by regulating mitochondrial quality control via HRedox biology · 2026Article
- Dynamic Organelle Remodeling in HIV-Associated Myocardial Disease: Mechanisms, Fibrotic Pathways, and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Advances in natural compounds modulating autophagy for the therapeutic intervention of heart failure.Molecular and cellular biochemistry · 2026Review
- Butyrate ameliorates doxorubicin-induced heart failure by inhibiting cardiomyocyte ferroptosis through the gut-heart axis.iScience · 2026Article
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Disulfidptosis in heart failure: an emerging mechanism awaiting exploration.Frontiers in cardiovascular medicine · 2026Review
- Review
- Vitamin C as a Cardioprotective Agent Against Doxorubicin-Induced Cardiotoxicity.Journal of the American Heart Association · 2025Review
- Class III Phosphatidylinositol-3 Kinase/Vacuolar Protein Sorting 34 in Cardiovascular Health and Disease.Journal of cardiovascular translational research · 2025Review
- Mitochondrial Amount Determines Doxorubicin-Induced Cardiotoxicity in Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The mTOR Signaling Pathway: Key Regulator and Therapeutic Target for Heart Disease.Biomedicines · 2025Review
- CircRNA CDR1AS promotes cardiac ischemia-reperfusion injury in mice by triggering cardiomyocyte autosis.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Chinese medicine targets cellular autophagy against cardiovascular diseases: research progress and future prospects.Frontiers in cardiovascular medicine · 2025Review
- eEF2K alleviates doxorubicin-induced cardiotoxicity by inhibiting GSK3β and improving autophagy dysfunction.Cell biology and toxicology · 2024Article
- Curcumin pretreatment attenuates myocardial ischemia/reperfusion injury by inhibiting ferroptosis, autophagy and apoptosis via HES1.International journal of molecular medicine · 2024Article
- Identification and validation of autophagy‑related genes in hypertrophic cardiomyopathy.Experimental and therapeutic medicine · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Autophagy mediates cellular quality control mechanisms and energy homeostasis through lysosomal degradation. Autophagy is typically viewed as an adaptive process that allows cells to survive against stress, such as nutrient deprivation and hypoxia. However, autophagy also mediates cell death during development and in response to stress. Cell death accompanied by autophagy activation and accumulation of autophagosomes has been classified as type II programmed cell death. Compared to the wealth of knowledge regarding the adaptive role of autophagy, however, the molecular mechanisms through which autophagy induces cell death and its functional significance are poorly understood. Autophagy is activated excessively under some conditions, causing uncontrolled degradation of cellular materials and cell death. An imbalance between autophagosome formation and lysosomal degradation causes a massive accumulation of autophagosomes, which subsequently causes cellular dysfunction and death. Dysregulation of autophagy induces a unique form of cell death, termed autosis, with defined morphological and biochemical features distinct from other forms of programmed cell death, such as apoptosis and necrosis. In the heart, dysregulated autophagy induces death of cardiomyocytes and actively mediates cardiac injury and dysfunction in some conditions, including reperfusion injury, doxorubicin cardiomyopathy, and lysosomal storage disorders. The goal in this review is to introduce the concept of autophagic cell death and discuss its functional significance in various cardiac conditions.
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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.