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压力超负荷肥厚型心肌病中心肌细胞程序性细胞死亡的研究进展

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

作者信息

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

机构信息

Department of Anesthesiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029, China.

Department of Emergency, The State Key Laboratory for Complex, Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100730, China.

出版信息

Apoptosis. 2025 Aug 14. doi: 10.1007/s10495-025-02146-5.

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.

摘要

压力超负荷肥厚型心肌病(PO-HCM)是一种常见的心血管疾病,其特征是心脏对慢性压力超负荷的适应性反应。然而,过度的压力超负荷会导致心肌细胞功能障碍和病理性肥大。PO-HCM的病理特征包括心肌细胞异常增大(肥大)和心肌组织的结构重塑。其发病机制是多方面的,涉及血流动力学改变、神经体液调节失衡和细胞内信号通路异常。在这种病理背景下,程序性细胞死亡在心肌细胞中起着关键作用。本综述综合了目前关于PO-HCM中程序性细胞死亡机制的研究,包括凋亡、坏死性凋亡、焦亡、自噬和铁死亡,以为转化研究提供信息并指导未来的治疗发展。

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