心房颤动
医学
不利影响
酪氨酸激酶
能量代谢
药理学
线粒体
酪氨酸激酶抑制剂
内科学
生物
受体
癌症
细胞生物学
作者
Yukun Li,Xiaodong Peng,Rong Lin,Xuesi Wang,Xinmeng Liu,Fanchao Meng,Yanfei Ruan,Rong Bai,Ribo Tang,Nian Liu
标识
DOI:10.15212/cvia.2023.0070
摘要
Tyrosine kinase inhibitors (TKIs) are a novel category of antitumor agents with remarkable efficacy in extending patient survival. However, clinical use of TKIs has been hindered by the major adverse effect of atrial fibrillation (AF). Recent studies have revealed that TKIs induce metabolic alterations and remodeling in cardiomyocytes, thus perturbing energy metabolism. Specifically, mitochondrial dysfunction and shifts in cardiac substrate utilization have been implicated in the mechanisms underlying TKI-induced AF. In light of these findings, this article reviews the energy metabolism-associated pathways involved in TKI-induced AF, identifies precise therapeutic targets for managing this condition, and discusses evidence that may contribute to the development of novel TKIs without cardiac adverse effects.
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