血糖异常、细胞死亡与心肌梗死

Dysglycemia, cell death and myocardial infarction

摘要:

细胞死亡是各种疾病导致机体损伤与修复的重要细胞学机制，其3种主要形式（坏死、凋亡和自噬）均参与了心肌梗死的病理生理过程。血糖异常，无论是高血糖还是低血糖，都会导致心肌梗死患者发病率和死亡率升高，但机制不明。本综述通过对细胞死亡的分类与机制、细胞死亡与心肌梗死的关系，以及血糖异常对梗死心肌细胞死亡的调节作用进行总结和分析，得出血糖异常导致心肌梗死预后不良可能是通过调节心肌细胞死亡而实现。因此，对于心肌梗死合并血糖异常的患者，人为地干预心肌细胞死亡通路的不同环节有望成为改善心肌梗死患者预后的新方法。

Abstract:

Cell death is the important cytological mechanism for organ injury and repair resulting from various diseases, and its 3 forms, necrosis, apoptosis and autophagy, are all involved in the pathophysical development of myocardial infarction (MI). Dysglycemia, not matter hyperglycemia or hypoglycemia is associated with higher morbidity and mortality in patients with MI. However, there are few studies focusing on the relationships among cell death, dysglycemia and MI. In this review, we summarized the mechanisms of cell death, the role of cell death in MI and the regulatory effects of dysglycemia in myocardial cell death. We brought forward that hyperglycemia and hypoglycemia can induce myocardial cell death, which plays a significant role in the development of MI through different pathways. Dysglycemia might induce poor prognosis after MI through regulating myocardial cell death. Therefore, for the MI patients with dysglycemia, regulation of the pathways of myocardial cell death, might be a new approach to improve prognosis of MI patients.