Lysyl oxidase-like 2 inhibitor rescues D-galactose-induced skeletal muscle fibrosis

作者全名:"Wu, Yongxin; Wu, Yaoxuan; Yang, Yunfei; Yu, Jing; Wu, Jianghao; Liao, Zhiyin; Guo, Ai; Sun, Yue; Zhao, Yuxing; Chen, Jinliang; Xiao, Qian"

作者地址:"[Wu, Yongxin; Wu, Yaoxuan; Yang, Yunfei; Yu, Jing; Wu, Jianghao; Liao, Zhiyin; Guo, Ai; Sun, Yue; Zhao, Yuxing; Chen, Jinliang; Xiao, Qian] Chongqing Med Univ, Affiliated Hosp 1, Dept Geriatr, Chongqing, Peoples R China"

通信作者:"Xiao, Q (通讯作者),Chongqing Med Univ, Affiliated Hosp 1, Dept Geriatr, Chongqing, Peoples R China."

来源:AGING CELL

ESI学科分类:MOLECULAR BIOLOGY & GENETICS

WOS号:WOS:000812158400001

JCR分区:Q1

影响因子:7.8

年份:2022

卷号: 

期号: 

开始页: 

结束页: 

文献类型:Article; Early Access

关键词:aging; LOXL2; mitochondria; sarcopenia; senescence; skeletal muscle

摘要:"Aging-related sarcopenia is currently the most common sarcopenia. The main manifestations are skeletal muscle atrophy, replacement of muscle fibers with fat and fibrous tissue. Excessive fibrosis can impair muscle regeneration and function. Lysyl oxidase-like 2 (LOXL2) has previously been reported to be involved in the development of various tissue fibrosis. Here, we investigated the effects of LOXL2 inhibitor on D-galactose (D-gal)-induced skeletal muscle fibroblast cells and mice. Our molecular and physiological studies show that treatment with LOXL2 inhibitor can alleviate senescence, fibrosis, and increased production of reactive oxygen species in fibroblasts caused by D-gal. These effects are related to the inhibition of the TGF-beta 1/p38 MAPK pathway. Furthermore, in vivo, mice treatment with LOXL2 inhibitor reduced D-gal-induced skeletal muscle fibrosis, partially enhanced skeletal muscle mass and strength and reduced redox balance disorder. Taken together, these data indicate the possibility of using LOXL2 inhibitors to prevent aging-related sarcopenia, especially with significant fibrosis."

基金机构:"National Natural Science Foundation of China [81901424, 82101652]"

基金资助正文:"National Natural Science Foundation of China, Grant/Award Number: 81901424 and 82101652"