The role of NLRP3 inflammasome in inflammation-related skeletal muscle atrophy

作者：Yukun Liu, Dongfang Wang, Tianyu Li, Fan Yang, Zhanfei Li, Xiangjun Bai, Yu-Chang Wang · 发表于：Frontiers in Immunology · 年份：2022 · DOI：10.3389/fimmu.2022.1035709 · 被引用次数：53 · 研究领域：Inflammasome and immune disorders、Exercise and Physiological Responses、Thermal Regulation in Medicine

Skeletal muscle atrophy is a common complication in survivors of sepsis, which affects the respiratory and motor functions of patients, thus severely impacting their quality of life and long-term survival. Although several advances have been made in investigations on the pathogenetic mechanism of sepsis-induced skeletal muscle atrophy, the underlying mechanisms remain unclear. Findings from recent studies suggest that the nucleotide-binding and oligomerisation domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, a regulator of inflammation, may be crucial in the development of skeletal muscle atrophy. NLRP3 inhibitors contribute to the inhibition of catabolic processes, skeletal muscle atrophy and cachexia-induced inflammation. Here, we review the mechanisms by which NLRP3 mediates these responses and analyse how NLRP3 affects muscle wasting during inflammation.