SESN2/sestrin2 suppresses sepsis by inducing mitophagy and inhibiting NLRP3 activation in macrophages
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Cites background from "SESN2/sestrin2 suppresses sepsis by..."
...Recently, Nomura et al. demonstrated that MSU crystals induced K+ efflux, leading to a Ca2+ influx-dependent depolarization of mitochondrial membrane potential and decreased intracellular ATP concentration (126)....
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...However, The NLRP3 is activated by wide range of bacterial, viral, and fungal PAMPs and endogenous DAMPs, such as pore-forming toxins, crystals, aggregates (such as β-amyloid), extracellular ATP, and hyaluronan (32)....
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...SESN2 was also demonstrated to be required for mitophagy through mitochondrial priming and autophagosome formation and to suppress prolonged inflammasome activation in macrophages treated with LPS and ATP (87)....
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...SESN2-deficient mice had higher serum levels of pro-inflammatory cytokines IL-1β and IL-18, elevated organ dysfunction and higher mortality rate in CLP- and LPS-induced sepsis (87)....
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...It was reported that mitochondrial ROS production and subsequent mitochondrial membrane permeability transition (MPT) leads to translocation of mtDNA into the cytosol after LPS and ATP treatment (82)....
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