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目前,越来越多的研究表明Rac1分子在心房纤维化及心房结构重构中发挥着重要作用。激活后的Rac1可以引起烟酰胺腺嘌呤二核苷酸磷酸氧化酶、结缔组织生长因子、N-钙粘蛋白、缝隙连接蛋白43、赖氨酰氧化酶等表达上调,同时还可以激活Janus激酶/信号转导子和转录激活子、凋亡信号调节激酶1/核因子-κB等信号途径,最终导致心房肌细胞氧化应激负荷增加、心肌细胞肥厚、间质纤维化、心房电传导紊乱、细胞间连接的异常分布等改变,从而促进心房重构形成,利于心房颤动的发生。已有的研究还提示他汀类药物可能通过干预Rac1的激活,成为心房颤动防治的新方法。
At present, more and more researches show that Rac1 plays an important role in atrial fibrosis and atrial remodeling. The activated Rac1 can cause nicotinamide adenine dinucleotide phosphate oxidase, connective tissue growth factor, N-cadherin, connexin43, lysyl oxidase expression upregulation, but also can activate Janus kinase / Signal transducer and activator of transcription, apoptosis signaling regulates kinase 1 / nuclear factor-kappaB and other signaling pathways leading to increased oxidative stress load in atrial myocytes, cardiomyocyte hypertrophy, interstitial fibrosis, atrial electrical conduction disturbance, Anomalous changes in the connection between the changes in order to promote the formation of atrial remodeling, which will help the occurrence of atrial fibrillation. Existing research also suggests that statins may become a new method of prevention and treatment of atrial fibrillation by interfering with the activation of Rac1.