摘要
Tyrosine kinase inhibitors(TKIs)are a novel category of antitumor agents with remarkable efficacy in extending pa-tient 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 perturb-ing 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 ef-fects.
基金
This work was supported by the National Science Foundation of China(grant No.81770318)
Beijing Municipal Natural Science Foundation(grant No.7192051).
