Irisin ameliorates D-galactose-induced skeletal muscle fibrosis via the PI3K/Akt pathway

作者全名："Wu, Yaoxuan; Wu, Yongxin; Yu, Jing; Zhang, Yingxiao; Li, Yuanfen; Fu, Rao; Sun, Yue; Zhao, Kexiang; Xiao, Qian"

作者地址："[Wu, Yaoxuan; Wu, Yongxin; Yu, Jing; Zhang, Yingxiao; Li, Yuanfen; Fu, Rao; Sun, Yue; Zhao, Kexiang; Xiao, Qian] Chongqing Med Univ, Dept Geriatr, Affiliated Hosp 1, Chongqing, Peoples R China; [Zhao, Kexiang] Chongqing Med Univ, Dept Geriatr, Affiliated Hosp 1, 1st You Yi Rd, Chongqing 400010, Peoples R China"

通信作者："Zhao, KX (通讯作者)，Chongqing Med Univ, Dept Geriatr, Affiliated Hosp 1, 1st You Yi Rd, Chongqing 400010, Peoples R China."

来源：EUROPEAN JOURNAL OF PHARMACOLOGY

ESI学科分类：PHARMACOLOGY & TOXICOLOGY

WOS号：WOS:000908787000001

JCR分区：Q1

影响因子：4.2

年份：2023

卷号：939

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：Irisin; Fibrosis; Redox imbalance; Aging; Sarcopenia

摘要："Primary sarcopenia is a multicausal skeletal muscle disease associated with muscle strength and mass loss. Skeletal muscle fibrosis is one of the significant pathological manifestations associated with the development of age-related sarcopenia. Irisin, which is cleaved by the extracellular domain of fibronectin type III domain containing protein 5 (FNDC5), has previously been reported to exert antifibrotic effects on the heart, liver, and pancreas, but whether it can rescue skeletal muscle fibrosis remains unknown. In this study, we examined the effects of irisin on D-galactose (D-gal)-induced skeletal muscle fibroblasts. We found that D-gal-induced senescence, fibrosis, and redox imbalance were inhibited by irisin treatment. Mechanistically, irisin or FNDC5 overexpression attenuated D-gal-induced senescence, redox imbalance, and fibrosis by regulating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. Overall, irisin might be a promising therapeutic candidate for age-related skeletal muscle fibrosis."

基金机构："National Natural Science Foundation of China; Post-doctoral Science Foundation of Chongqing, China; [81901424]; [2022TQ0398]"

基金资助正文："This work was financially supported by funding from the National Natural Science Foundation of China (No. 81901424) and the Post-doctoral Science Foundation of Chongqing, China (Grant Number: 2022TQ0398) ."