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<p>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.</p>

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Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年8月14日

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  • Fei Xiao,
  • Hui-Li Li,
  • Jia-Rui Wang,
  • Hui-Min Wu,
  • Yu-Qi Cai,
  • Jia-Wan Wang,
  • Hao Che,
  • Gang Li,
  • Zheng-Yuan Xia,
  • Yu-Bo Xie,
  • Sheng Wang

摘要

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.