Autophagic degradation of CCN2 (cellular communication network factor 2) causes cardiotoxicity of sunitinib
Zhifei Xu, Ying Jin, Zizheng Gao, Yan Zeng, Jiangxia Du, Hao Yan, Xueqin Chen, Ping Li, Nengming Lin, Bo Yang, Qiaojun He, Peihua Luo
Abstract
(high mobility group box 1) inhibited sunitinib-induced cardiomyocyte autophagy and apoptosis, and the HMGB1-specific inhibitor glycyrrhizic acid (GA) significantly mitigated sunitinib-induced autophagy, cardiomyocyte death and cardiotoxicity. Our study reveals a novel target protein of autophagic degradation in the regulation of cardiomyocyte death and highlights the pharmacological inhibitor of HMGB1 as an attractive approach for improving the safety of sunitinib-based cancer therapy.
Topics & Concepts
AutophagyCardiotoxicityBiologySunitinibDegradation (telecommunications)Cancer researchCell biologyCancerApoptosisBiochemistryGeneticsComputer scienceChemotherapyTelecommunicationsConnective Tissue Growth Factor Research