Wu Dongda, Deng Donghong, Tang Biao
Medical School, Hunan University of Chinese Medicine, 410208 Changsha, Hunan, China.
People's Hospital of Ningxiang City, Hunan University of Chinese Medicine, 410600 Changsha, Hunan, China.
Rev Cardiovasc Med. 2025 Jul 28;26(7):38407. doi: 10.31083/RCM38407. eCollection 2025 Jul.
Heart failure is a complex pathological condition characterized by various mechanisms of cellular death, among which programmed cell death (PCD) plays a crucial role in the pathophysiology of cardiac dysfunction. This review delves into the different forms of PCD present in heart failure, including apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis, and examines the mechanisms of action involved and the potential therapeutic targets for treating cardiac failure. By analyzing the latest research findings, we reveal the pivotal role of PCD in the progression of heart failure and discuss the preclinical prospects of intervening in these processes to develop novel therapeutic strategies. For instance, pharmacological agents that inhibit receptor-interacting protein kinases (RIPK1 and RIPK3) involved in necroptosis have been demonstrated to reduce cardiac injury and improve functional outcomes. Additionally, targeting the inflammatory responses associated with necrotic cell death, such as using interleukin (IL)-1β inhibitors, may provide a dual benefit by reducing cell death and inflammation. Thus, combining current knowledge will enhance our understanding in this field and promote innovative approaches to managing heart failure more effectively.
心力衰竭是一种复杂的病理状态，其特征在于多种细胞死亡机制，其中程序性细胞死亡（PCD）在心脏功能障碍的病理生理学中起着关键作用。本综述深入探讨了心力衰竭中存在的不同形式的PCD，包括凋亡、自噬、坏死性凋亡、焦亡和铁死亡，并研究了其涉及的作用机制以及治疗心力衰竭的潜在靶点。通过分析最新的研究结果，我们揭示了PCD在心力衰竭进展中的关键作用，并讨论了干预这些过程以开发新治疗策略的临床前前景。例如，已证明抑制参与坏死性凋亡的受体相互作用蛋白激酶（RIPK1和RIPK3）的药物可减少心脏损伤并改善功能结局。此外，靶向与坏死性细胞死亡相关的炎症反应，如使用白细胞介素（IL）-1β抑制剂，可能通过减少细胞死亡和炎症带来双重益处。因此，整合现有知识将增强我们对该领域的理解，并促进更有效地管理心力衰竭的创新方法。
