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心血管病是多种心脏和血管疾病的总称,包括心肌梗死和高血压等,是全球范围内造成死亡的第一位原因。转录因子叉头框蛋白O4(FoxO4)有多种生物学功能,参与了人类多种疾病的发生。最近,笔者研究团队发现了FoxO4在心肌梗死后左心室重构中的一种新功能。FoxO4可以通过内皮精氨酸酶1(arginase 1,Arg1)促进心肌梗死后早期炎症反应。缺血时,FoxO4可以激活内皮Arg1的转录,导致一氧化氮生成减少,单核细胞通过内皮屏障黏附和迁移增加。与野生型小鼠相比,FoxO4失活可以减轻心肌梗死后炎症反应,更好地保护心功能。根据FoxO4和Arg1之间的这种联系,推测FoxO4/Arg1/一氧化氮信号通路可能在高血压的发生过程中发挥着潜在的作用,因为Arg1和一氧化氮已被证实在血管生物学中发挥关键作用。FoxO4可能成为心肌梗死后心脏修复及血管疾病的潜在治疗靶点。
Cardiovascular disease is a general term for a variety of heart and vascular diseases, including myocardial infarction and high blood pressure, and is the leading cause of death worldwide. The transcription factor FoxO4 has several biological functions and is involved in many human diseases. Recently, the research team found a new function of FoxO4 in left ventricular remodeling after myocardial infarction. FoxO4 can promote early inflammatory reaction after myocardial infarction by arginase 1 (Arg1). During ischemia, FoxO4 activates the transcription of endothelial Arg1, resulting in reduced production of nitric oxide and increased monocyte adhesion and migration through the endothelial barrier. Compared with wild-type mice, inactivation of FoxO4 can reduce the inflammatory response after myocardial infarction and better protect heart function. Based on this association between FoxO4 and Arg1, it is speculated that the FoxO4 / Arg1 / nitric oxide signaling pathway may play a potential role in the pathogenesis of hypertension because Arg1 and nitric oxide have been shown to play a role in vascular biology Key role. FoxO4 may be a potential therapeutic target for cardiac repair and vascular disease after myocardial infarction.