ArticleEuropean journal of medical research2022
Inhibitors of IFN gene stimulators (STING) improve intestinal ischemia-reperfusion-induced acute lung injury by activating AMPK signaling.
Article in European journal of medical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Targeting STING to attenuate autophagy-mediated airway remodeling in asthma.Molecular and cellular biochemistry · 2026Article
- cGAS-STING targeting offers therapy choice in lung diseases.Biology direct · 2025Review
- Apigenin attenuates ischemia-reperfusion-induced pulmonary ferroptosis and fibrosis by activating the Nrf2/HO-1/GPX4 axis in mice.Turkish journal of biology = Turk biyoloji dergisi · 2025Article
- The Role of cGAS-STING Signalling in Metabolic Diseases: from Signalling Networks to Targeted Intervention.International journal of biological sciences · 2024Review
- Advancements in the study of acute lung injury resulting from intestinal ischemia/reperfusion.Frontiers in medicine · 2024Review
- Novel insight into cGAS-STING pathway in ischemic stroke: from pre- to post-disease.Frontiers in immunology · 2023Review
- cGAS-STING pathway in ischemia-reperfusion injury: a potential target to improve transplantation outcomes.Frontiers in immunology · 2023Review
- cGAS-STING signaling pathway in intestinal homeostasis and diseases.Frontiers in immunology · 2023Review
- The effect of the cyclic GMP-AMP synthase-stimulator of interferon genes signaling pathway on organ inflammatory injury and fibrosis.Frontiers in pharmacology · 2022Review
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute lung injury (ALI) caused by intestinal ischemia-reperfusion is a life-threatening disease. Interferon gene stimulator (STING) is a cytoplasmic DNA sensor that participates in the initiation of the inflammatory response. This study aims to establish whether C-176 (STING inhibitor) improves ALI under intestinal ischemia-reperfusion conditions.
methodsTo induce ALI, 72 male C57BL/6 mice were subjected to intestinal ischemia for 60 min and reperfusion for 3 h. Through intraperitoneal injection, C-176, a selective STING inhibitor, was injected 30 min before surgical treatment; meanwhile, compound C, an antagonist of adenosine monophosphate-activated protein kinase (AMPK), was administered 30 min after surgery. Based on immunofluorescence and Western blot assays, post-ALI assessments included lung water content (TLW), bronchoalveolar lavage fluid (BALF) protein, H&E staining, Masson staining, pulmonary pyroptosis [Gasdermin-D (GSDMD), cleaved caspase-1], and apoptosis (TUNEL, cleaved caspase-3).
resultsC-176 administration significantly attenuated intestinal ischemia-reperfusion-mediated ALI; this effect was reflected by exacerbated TLW and BALF protein, aggravated lung injury score, elevated degree of pulmonary fibrosis, increased TUNEL- and GSDMD-positive cells, and upregulated phospho-AMPK, cleaved caspase-1, cleaved caspase-3 and IFNβ mRNA expression. Moreover, C-176 increased phospho-AMPK under ALI conditions. Nonetheless, compound C partially reversed these beneficial effects.
conclusionC-176, a selective STING inhibitor, improves intestinal ischemia-reperfusion-mediated ALI, and its underlying mechanism may be associated with AMPK signal activation.
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