Open AccessHistone Deacetylase 2 Suppresses Skeletal Muscle Atrophy and Senescence via NF-κB Signaling Pathway in Cigarette Smoke-Induced Mice with Emphysema
Author(s) -
Chao Li,
Zhang Deng,
Guixian Zheng,
Ting Xie,
Xinyan Wei,
Zengyu Huo,
Jing Bai
Publication year - 2021
Publication title -
international journal of chronic obstructive pulmonary disease/international journal of copd
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.394
H-Index - 67
eISSN - 1178-2005
pISSN - 1176-9106
DOI - 10.2147/copd.s314640
Subject(s) - muscle atrophy , histone deacetylase 2 , medicine , skeletal muscle , endocrinology , gastrocnemius muscle , senescence , atrophy , copd , histone deacetylase , biology , histone , biochemistry , gene
Exposure to cigarette smoke (CS) is the main risk factor for chronic obstructive pulmonary disease (COPD). CS not only causes chronic airway inflammation and lung damage but also is involved in skeletal muscle dysfunction (SMD). Previous studies have shown that histone deacetylase 2 (HDAC2) plays an important role in the progression of COPD. The aim of this study was to determine the role of HDAC2 in CS-induced skeletal muscle atrophy and senescence.