Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol Via GSK3β Signaling Pathway

Overview

Journal EBioMedicine

Specialty Biomedical Engineering

Date 2017 Feb 6

PMID 28161398

Citations 16

Authors

Congcong Shen

Jin Zhou

Xiaoxiao Wang

Xi-Yong Yu

Chun Liang

Bin Liu

Xiangbin Pan

Qiong Zhao

Jenny Lee Song

Jiajun Wang

Meiyu Bao

Chaofan Wu

Yangxin Li

Yao-Hua Song

Affiliations

Soon will be listed here.

Abstract

While angiotensin II (ang II) has been implicated in the pathogenesis of cardiac cachexia (CC), the molecules that mediate ang II's wasting effect have not been identified. It is known TNF-α level is increased in patients with CC, and TNF-α release is triggered by ang II. We therefore hypothesized that ang II induced muscle wasting is mediated by TNF-α. Ang II infusion led to skeletal muscle wasting in wild type (WT) but not in TNF alpha type 1 receptor knockout (TNFR1KO) mice, suggesting that ang II induced muscle loss is mediated by TNF-α through its type 1 receptor. Microarray analysis identified cholesterol 25-hydroxylase (Ch25h) as the down stream target of TNF-α. Intraperitoneal injection of 25-hydroxycholesterol (25-OHC), the product of Ch25h, resulted in muscle loss in C57BL/6 mice, accompanied by increased expression of atrogin-1, MuRF1 and suppression of IGF-1/Akt signaling pathway. The identification of 25-OHC as an inducer of muscle wasting has implications for the development of specific treatment strategies in preventing muscle loss.

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