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The emerging role of stimulator of interferons genes signaling in sepsis: Inflammation, autophagy, and cell death
Author(s) -
Hu Qiongyuan,
Knight Patrick H.,
Ren Yanhan,
Ren Huajian,
Zheng Jiashuo,
Wu Xiuwen,
Ren Jianan,
Sawyer Robert G.
Publication year - 2019
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.13194
Subject(s) - pyroptosis , sting , autophagy , inflammation , sepsis , stimulator of interferon genes , necroptosis , signal transduction , immunology , programmed cell death , biology , microbiology and biotechnology , proinflammatory cytokine , medicine , cancer research , apoptosis , innate immune system , inflammasome , immune system , genetics , engineering , aerospace engineering
Stimulator of interferons genes (STING) is an adaptor protein that plays a critical role in the secretion of type I interferons and pro‐inflammatory cytokines in response to cytosolic nucleic acid. Recent research indicates the involvement of the STING pathway in uncontrolled inflammation, sepsis, and shock. STING signaling is significantly up‐regulated in human sepsis, and STING agonists are suggested to contribute to the pathogenesis of sepsis and shock. Nevertheless, little is known about the consequences of activated STING‐mediated signaling during sepsis. It has been shown that aberrant activation of the STING‐dependent way can result in increased inflammation, type I interferons responses, and cell death (including apoptosis, necroptosis, and pyroptosis). In addition, autophagy modulation has been demonstrated to protect against multiple organs injuries in animal sepsis model. However, impaired autophagy may contribute to the aberrant activation of STING signaling, leading to uncontrolled inflammation and cell death. Here we present a comprehensive review of recent advances in the understanding of STING signaling, focusing on the regulatory mechanisms and the roles of this pathway in sepsis.