ArticleImmunity, inflammation and disease2023
IL-38 attenuates myocardial ischemia-reperfusion injury by inhibiting macrophage inflammation.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 16 citations in OpenAlex.
- Inflammaging and cytokine-driven cardiovascular senescence in age-related myocardial infarction: mechanisms, biomarkers, and precision immunotherapy strategies.Biogerontology · 2026Review
- Anti-Inflammatory Interleukins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2026Review
- Inflammation and wound healing: a comprehensive overview of mechanisms, therapeutic strategies, and translational perspectives.Biomarker research · 2026Review
- Macrophage polarization in ischemia-reperfusion injury: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- [Exosome-derived miR-1275 mediates IL-38 upregulation in lymphocytes to suppress lipopolysaccharide-induced apoptosis of myocardial cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Interleukin-38 as a potential diagnostic biomarker for heart failure.Biomarkers in medicine · 2025Article
- Notoginsenoside R1 Attenuates H/R Injury in H9c2 Cells by Maintaining Mitochondrial Homeostasis.Current issues in molecular biology · 2025Article
- Dichotomous roles of IL-36 and IL-38 in cardiovascular disease.Frontiers in immunology · 2025Review
- Lactate-Induced Mitochondrial Calcium Uptake 3 Aggravates Myocardial Ischemia-Reperfusion Injury by Promoting Neutrophil Extracellular Trap Formation.Research (Washington, D.C.) · 2025Article
- High‑fat diet‑induced LCN2 exacerbates myocardial ischemia‑reperfusion injury by enhancing platelet activation.Molecular medicine reports · 2024Article
- The interplay between T lymphocytes and macrophages in myocardial ischemia/reperfusion injury.Molecular and cellular biochemistry · 2024Review
- Article
- The effect of macrophages and their exosomes in ischemic heart disease.Frontiers in immunology · 2024Review
- Role of IL-1 Family Cytokines IL-36, IL-37, IL-38 in Osteoarthritis and Rheumatoid Arthritis: A Comprehensive Review.Journal of inflammation research · 2024Review
- The emerging role of IL-38 in diseases: A comprehensive review.Immunity, inflammation and disease · 2023Review
- IL-38 attenuates myocardial ischemia-reperfusion injury by inhibiting macrophage inflammation.Immunity, inflammation and disease · 2023Article
- Macrophage Heterogeneity and Its Impact on Myocardial Ischemia-Reperfusion Injury: An Integrative Review.Journal of inflammation research · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundReperfusion therapy is the most effective approach to resolve coronary occlusion, but myocardial injury caused by excessive inflammation during myocardial ischemia-reperfusion will also pose a new threat to health. Our prior study revealed the expression pattern of interleukin-38 (IL-38) in the peripheral blood serum of patients with ischemic cardiomyopathy and the role of IL-38 in acute myocardial infarction in mice. However, its role and potential mechanisms in myocardial ischemia/reperfusion injury (MIRI) remain to be determined. METHODS AND
resultsThe left anterior descending artery of C57BL/6 mice was transiently ligated to induce the MIRI model. We found that MIRI induced the expression of endogenous IL-38, which was mainly produced by locally infiltrating macrophages. Overexpression of IL-38 in C57BL/6 mice attenuated inflammatory injury and decreased myocardial apoptosis after myocardial ischemia-reperfusion. Furthermore, IL-38 inhibited lipopolysaccharide-induced macrophage inflammation in vitro. Cardiomyocytes cocultured with the supernatant of IL-38- and troponin I-treated macrophages showed a lower rate of apoptosis than controls.
conclusionsIL-38 attenuates MIRI by inhibiting macrophage inflammation. This inhibitory effect may be partially achieved by inhibiting the activation of NOD-like receptor pyrin domain-related protein 3 inflammasome, resulting in decreased expression of inflammatory factors and reduced cardiomyocyte apoptosis.
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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 OpenQuestion graph.