mtDNA-STING pathway promotes necroptosis-dependent enterocyte injury in intestinal ischemia reperfusion

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STING-mediated intestinal barrier dysfunction contributes to lethal sepsis

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Autophagy induction via STING trafficking is a primordial function of the cGAS pathway

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Ischemia-induced ACSL4 activation contributes to ferroptosis-mediated tissue injury in intestinal ischemia/reperfusion

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Mitochondrial Damage and Activation of the STING Pathway Lead to Renal Inflammation and Fibrosis

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PUMA amplifies necroptosis signaling by activating cytosolic DNA sensors

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Targeting the miR-665-3p-ATG4B-autophagy axis relieves inflammation and apoptosis in intestinal ischemia/reperfusion

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Released Mitochondrial DNA Following Intestinal Ischemia Reperfusion Induces the Inflammatory Response and Gut Barrier Dysfunction

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The cytosolic sensor STING is required for intestinal homeostasis and control of inflammation

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Systemic blockade of P2X7 receptor protects against sepsis-induced intestinal barrier disruption

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miR-34a-5p Inhibition Alleviates Intestinal Ischemia/Reperfusion-Induced Reactive Oxygen Species Accumulation and Apoptosis via Activation of SIRT1 Signaling

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Necroptosis is a key mediator of enterocytes loss in intestinal ischaemia/reperfusion injury

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Red Blood Cells Induce Necroptosis of Lung Endothelial Cells and Increase Susceptibility to Lung Inflammation

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Redefining the gut as the motor of critical illness

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Chemokines and mitochondrial products activate neutrophils to amplify organ injury during mouse acute liver failure

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Gastrointestinal function in intensive care patients: terminology, definitions and management. Recommendations of the ESICM Working Group on Abdominal Problems

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Circulating mitochondrial DAMPs cause inflammatory responses to injury

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Local and remote tissue injury upon intestinal ischemia and reperfusion depends on the TLR/MyD88 signaling pathway

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STING is an endoplasmic reticulum adaptor that facilitates innate immune signalling

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