心肌梗死中涉及炎症和凋亡的机制

The mechanisms of inflammation and apoptosis in myocardial infarction

由心肌梗死引起的炎症反应和细胞凋亡对病程的发展和预后有着极其重要的作用,炎症可以通过肿瘤坏死因子α(TNF-α)、CCAAT/增强子结合蛋白同源蛋白(CHOP)、白细胞介素10(IL-10)、α7烟酸型乙酰胆碱受体(α7nAChR)信号途径对细胞的凋亡进行调控,凋亡反馈可影响炎症的严重程度,两者共同影响了心肌梗死面积的大小和心功能的恢复。抑制炎症和减少凋亡已经成为心肌梗死后预防心室重构、调节心功能紊乱的重要环节,对其深入研究具有广阔的前景。

The inflammation and apoptosis were vital important in the progress and recovery in myocardial infarction.Apoptosis was regulated by inflammation though TNF-α,CHOP,IL-10andα7nAChR signal pathways and influenced the severity of the inflammation viafeedback regulation.Inflammation and apoptosis affected myocardial infarction size and cardiac function recovery together.Inhibition of inflammation,reducing apoptosis had been proved to be the important parts in prevention of ventricular remodeling and regulating cardiac dysfunction after myocardial infarction,which had broad prospects.