自噬在急性心肌梗死发病中作用的研究进展

Research progress of the Role of Autophagy in the Pathogenesis and Progression of Acute Myocardial Infarction

自噬是生物细胞内普遍存在且高度保守的一种生理过程,其通过溶酶体融合降解细胞内的大分子组分、受损的细胞器以及侵入胞内的病原菌,以达到维持细胞稳态的目的。自噬在多种疾病的发生发展中也发挥十分重要的作用,尤其是心血管疾病。自噬对其病程的发展可以发挥两种截然不同的作用。适当的自噬作用可以降低炎症反应和氧化应激促进细胞的存活,以及通过减少泡沫细胞的形成而对维持心血管的正常功能起一个保护作用;但过度的自噬作用会对细胞造成不可逆的损伤,诱导细胞发生不依赖于caspase的自噬性细胞死亡,增加局部的炎症反应,从而促进动脉粥样硬化病变的发展。本文就自噬在急性心肌梗死发生发展中作用的研究进展进行了综述,探讨自噬成为预防及治疗心血管疾病新靶标的可能性。

Autophagy is a prevalent and highly conservedphysiological process which is characterized by the lysosome-dependent degradation of intracellular components, damaged organelles and invasive pathogens to maintain cellular homeostasis. Autophagy plays a key role in pathogenesis and development of diseases. In particular, autophagy plays dual roles in the cardiovascular diseases. Physiological autophagy is a protective factor to maintain normal cardiovascular function either by reducing inflammatory responses and oxidative stresses to promote cell survival, or by lessening the formation of foam cells. On the other hand,excessive autophagy may cause irreversible damages to cells to induce caspase-independent autophagic cell death, thusaugmenting local inflammatory responses to accelerate the development of atherosclerotic lesions. This article mainly reviews the dual role of autophagy in the pathological processes of acute myocardial infarction and investigate the possibility of autophagy to be a new target for prevention and management of cardiovascular diseases.