ArticlePloS one2026
Multi-omics analysis reveals STING activation mediates NLRP3-related pyroptosis and exacerbates myocardial ischemia-reperfusion injury.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research Progress on Anti-Inflammatory Adipokine SFRP5-Mediated Lipid Metabolism and Its Potential Role in Neural Development.Immunity, inflammation and disease · 2026Pooled it
- Direct NLRP3 inflammasome inhibitors for cardiovascular therapeutics: a comparative review of synthetic and natural candidates.Frontiers in pharmacology · 2026Review
- Neutrophil-mediated myocardial ischemia-reperfusion injury: mechanisms and potential therapeutic targets.Frontiers in immunology · 2026Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial ischemia-reperfusion injury (I/R) significantly exacerbates cardiomyocyte damage post-recanalization therapy in acute myocardial infarction. Pyroptosis and the NLRP3 inflammasome are crucial in I/R, yet the precise mechanism remains unclear. MATERIALS AND
methodsTranscriptomics, proteomics, and single-cell transcriptomics were employed to examine cellular subtype changes and pyroptosis-associated gene regulation in I/R. Differential pyroptosis-related genes were identified from transcriptomics data and validated with proteomics. Single-cell RNA sequencing assessed pyroptosis levels and intercellular communication. Mouse myocardial I/R and human cardiomyocyte hypoxia/reoxygenation (H/R) models were used to explore STING overexpression/silencing effects on NLRP3 inflammasome activation, oxidative stress, and cellular injury.
resultsPyroptosis-related genes were significantly dysregulated, implicating multiple inflammatory pathways. Single-cell analyses revealed increased granulocytes, macrophage infiltration, cardiomyocyte injury, and enhanced pyroptosis scores post-I/R. Cardiomyocytes, endothelial cells, and fibroblasts exhibited increased pyroptosis and inflammatory cell-cell interactions. Animal studies indicated significant declines in cardiac function and increased oxidative stress and inflammation post-I/R. STING activation (SR717) worsened cardiac function, enhanced ROS production, and elevated myocardial injury markers; STING inhibition (H151) markedly mitigated these effects. Correspondingly, the cGAS-STING pathway and NLRP3 inflammasome factors were significantly upregulated post-I/R, exacerbated by STING agonists and alleviated by STING inhibitors. Cellular studies confirmed that STING overexpression intensified oxidative stress and pyroptosis, effects reversed by STING knockdown and blocked by NLRP3 inhibitor MCC950.
conclusionSTING activation contributes to oxidative stress and NLRP3 inflammasome-associated pyroptosis during I/R. Targeting the STING-NLRP3 axis may represent a potential strategy to reduce myocardial injury after ischemia-reperfusion.
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