ArticleScientific reports2026
Protective role of IRG1/itaconate in acute myocardial injury: association with NLRP3 inflammasome and oxidative stress.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Immunoresponsive Gene 1-Itaconate Exacerbates Hypertension by Inhibiting the Cystathionine Gamma-Lyase/Hydrogen Sulfide Pathway.Journal of cardiovascular development and disease · 2026Article
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Increasing evidence indicates the critical role of Immune response gene 1 (IRG1)-derived itaconate in metabolic regulation and signal transduction, with therapeutic implications for inflammatory diseases. However, its mechanistic involvement in acute myocardial injury remains unclear. This study investigated the protective effects of itaconate in LPS-induced acute myocardial injury. LPS exposure upregulated IRG1 expression and levels of itaconate in murine cardiac tissue, while IRG1 deficiency exacerbated myocardial inflammation (elevated BNP, CK-MB, TNF-α, IL-6, and MPO activity), cardiac dysfunction, and mortality. Mechanistically, IRG1 absence promoted NLRP3 inflammasome activation and oxidative stress. Administration of 4-octyl itaconate (4-OI), a cell-permeable itaconate derivative, mitigated LPS-induced acute myocardial injury, reduced pro-inflammatory cytokines, and improved cardiac function in both wild-type (WT) and IRG1 knockout (KO) mice. 4-OI also modulated oxidative stress and Nrf2 signaling. These findings demonstrate that IRG1/itaconate exerts protective effects in acute myocardial injury, and 4-OI may have the potential to prevent sepsis-related acute myocardial injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.