Regulation of Autophagy, Apoptosis, and Cell Death in Cardiomyocytes and Potential Therapeutic Targets
- 1Department of Cardiology, Jilin People’s Hospital, 132001 Jilin, Jilin, China
- 2The Center of Cardiology, Affiliated Hospital, Beihua University, 132011 Jilin, Jilin, China
Abstract
Disruption of cardiomyocyte homeostasis is a fundamental pathological basis for the onset and progression of cardiovascular diseases (CVDs). Given the extremely limited regenerative capacity of cardiomyocytes, programmed cell death (PCD) has emerged as a critical determinant of disease pathogenesis and clinical outcomes. PCD comprises multiple forms of cell death, including necroptosis, pyroptosis, ferroptosis, cuproptosis, disulfidptosis, necrosis induced by sodium overload (NECSO), lysosomal cell death, oxeiptosis, PANoptosis, entotic cell death, netotic cell death, alkaliptosis, and poly(ADP-ribose) polymerase-1 (PARP-1)-dependent cell death (parthanatos). Complex molecular interactions and signaling crosstalk among these cell death pathways can lead to the dysregulation of these pathways and, in turn, induce various CVDs. Currently, the mechanisms linking cardiomyocyte PCD to CVDs remain incompletely understood. Therefore, this article systematically reviews advances in research over the past decade on autophagy, apoptosis, necrosis, and other forms of PCD in cardiomyocytes. Moreover, this review summarizes the molecular mechanisms and pathway interaction networks underlying these cell death modalities, examines key regulatory targets and the potential to develop and translate targeted inhibitors into clinical practice, and outlines strategies for targeted intervention in cardiomyocyte PCD to prevent and treat CVDs. Collectively, this review aims to provide a theoretical foundation for further research into precision therapies for heart diseases.
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BibTeX
@article{feng2026regulation,
title = {{Regulation of Autophagy, Apoptosis, and Cell Death in Cardiomyocytes and Potential Therapeutic Targets}},
author = {Xing Feng and Ye Wang and Tangna Sun and Tongku Liu},
journal = {Reviews in Cardiovascular Medicine},
year = {2026},
month = oct,
doi = {10.31083/rcm52423},
url = {https://doi.org/10.31083/rcm52423},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Regulation of Autophagy, Apoptosis, and Cell Death in Cardiomyocytes and Potential Therapeutic Targets
AU - Xing Feng
AU - Ye Wang
AU - Tangna Sun
AU - Tongku Liu
PY - 2026
DA - 2026/10/10
JO - Reviews in Cardiovascular Medicine
DO - 10.31083/rcm52423
UR - https://doi.org/10.31083/rcm52423
AB - Disruption of cardiomyocyte homeostasis is a fundamental pathological basis for the onset and progression of cardiovascular diseases (CVDs). Given the extremely limited regenerative capacity of cardiomyocytes, programmed cell death (PCD) has emerged as a critical determinant of disease pathogenesis and clinical outcomes. PCD comprises multiple forms of cell death, including necroptosis, pyroptosis, ferroptosis, cuproptosis, disulfidptosis, necrosis induced by sodium overload (NECSO), lysosomal cell death, oxeiptosis, PANoptosis, entotic cell death, netotic cell death, alkaliptosis, and poly(ADP-ribose) polymerase-1 (PARP-1)-dependent cell death (parthanatos). Complex molecular interactions and signaling crosstalk among these cell death pathways can lead to the dysregulation of these pathways and, in turn, induce various CVDs. Currently, the mechanisms linking cardiomyocyte PCD to CVDs remain incompletely understood. Therefore, this article systematically reviews advances in research over the past decade on autophagy, apoptosis, necrosis, and other forms of PCD in cardiomyocytes. Moreover, this review summarizes the molecular mechanisms and pathway interaction networks underlying these cell death modalities, examines key regulatory targets and the potential to develop and translate targeted inhibitors into clinical practice, and outlines strategies for targeted intervention in cardiomyocyte PCD to prevent and treat CVDs. Collectively, this review aims to provide a theoretical foundation for further research into precision therapies for heart diseases.
SN - 1530-6550
SN - 2153-8174
ER -