Programmed Cell Death Pathways in the Pathogenesis of Idiopathic Inflammatory Myopathies

Idiopathic inflammatory myopathy (IIM) is a heterogeneous group of acquired, autoimmune muscle diseases characterized by muscle inflammation and extramuscular involvements. Present literatures have revealed that dysregulated cell death in combination with impaired elimination of dead cells contribut...

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Published inFrontiers in immunology Vol. 12; p. 783616
Main Authors Shi, Jia, Tang, Mingwei, Zhou, Shuang, Xu, Dong, Zhao, Jiuliang, Wu, Chanyuan, Wang, Qian, Tian, Xinping, Li, Mengtao, Zeng, Xiaofeng
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 24.11.2021
Subjects
Alarmins - immunology
Alarmins - metabolism
Animals
apoptosis
Autoantigens - immunology
Autoantigens - metabolism
autophagy
Cytokines - immunology
Cytokines - metabolism
Humans
idiopathic inflammatory myopathy (IIM)
Immunology
Inflammation Mediators - immunology
Inflammation Mediators - metabolism
Muscle, Skeletal - immunology
Muscle, Skeletal - metabolism
Muscle, Skeletal - pathology
Myositis - immunology
Myositis - metabolism
Myositis - pathology
NETosis
programmed cell death (PCD)
pyroptosis
Regulated Cell Death
Signal Transduction
pyroptosis
apoptosis
idiopathic inflammatory myopathy (IIM)
NETosis
autophagy
programmed cell death (PCD)
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Summary:Idiopathic inflammatory myopathy (IIM) is a heterogeneous group of acquired, autoimmune muscle diseases characterized by muscle inflammation and extramuscular involvements. Present literatures have revealed that dysregulated cell death in combination with impaired elimination of dead cells contribute to the release of autoantigens, damage-associated molecular patterns (DAMPs) and inflammatory cytokines, and result in immune responses and tissue damages in autoimmune diseases, including IIMs. This review summarizes the roles of various forms of programmed cell death pathways in the pathogenesis of IIMs and provides evidence for potential therapeutic targets.
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SourceType-Scholarly Journals-1
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ObjectType-Review-3
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Reviewed by: Tsutomu Takeuchi, Keio University, Japan; Yikun Yao, National Institutes of Health (NIH), United States
Edited by: Zhiyong Chen, Shanghai Sixth People’s Hospital, China
This article was submitted to Autoimmune and Autoinflammatory Disorders, a section of the journal Frontiers in Immunology
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2021.783616