ArticleJCI insight2022
Targeting IL-36 improves age-related coronary microcirculatory dysfunction and attenuates myocardial ischemia/reperfusion injury in mice.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Review
- Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.Immunogenetics · 2026Article
- Anti-Inflammatory Interleukins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2026Review
- Comparing anti-platelet and anti-thrombin therapies in the ischaemia-reperfusion injured coronary microcirculation of healthy and diabetic mice.Basic research in cardiology · 2026Article
- Targeting the Toll-Like Receptor 4 Ameliorates Heart Failure in Aged Mice by Inhibiting the Formation of Neutrophil Extracellular Traps.Physiological research · 2026Article
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Comparison of All-Cause Mortality in Generalized Pustular Psoriasis and Plaque Psoriasis: A Systematic Review and Meta-Analysis.Dermatology and therapy · 2026Article
- Upregulation and diagnostic potential of Interleukin-36 cytokine isoforms in dilated cardiomyopathy: evidence from human and murine models.Molecular biology reports · 2025Article
- Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025Review
- Impact of chronic hyperglycaemia on the coronary microcirculation - benefits of targeting IL-36 and diet reversal.Basic research in cardiology · 2025Article
- The predictive value of the neutrophil/platelet ratio on in-hospital adverse events and long-term prognosis in patients with coronary artery disease after percutaneous coronary intervention and its possible internal mechanism.Molecular and cellular biochemistry · 2024Article
- Expanding Role of Interleukin-1 Family Cytokines in Acute Ischemic Stroke.International journal of molecular sciences · 2024Review
- Combined inhibition of IL-1, IL-33 and IL-36 signalling by targeting IL1RAP ameliorates skin and lung fibrosis in preclinical models of systemic sclerosis.Annals of the rheumatic diseases · 2024Article
- Generalized Pustular Psoriasis and Systemic Organ Dysfunctions.International journal of molecular sciences · 2024Review
- Interleukin-1 receptor accessory protein blockade limits the development of atherosclerosis and reduces plaque inflammation.Cardiovascular research · 2024Article
- The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Monitoring coronary blood flow by laser speckle contrast imaging after myocardial ischaemia reperfusion injury in adult and aged mice.Frontiers in cardiovascular medicine · 2024Article
- Inflammation as the nexus: exploring the link between acute myocardial infarction and chronic obstructive pulmonary disease.Frontiers in cardiovascular medicine · 2024Review
- IL-17A-driven psoriasis is critically dependent on IL-36 signaling.Frontiers in immunology · 2023Article
- Improving vasculoprotective effects of MSCs in coronary microvessels - benefits of 3D culture, sub-populations and heparin.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Following myocardial infarction (MI), elderly patients have a poorer prognosis than younger patients, which may be linked to increased coronary microvessel susceptibility to injury. Interleukin-36 (IL-36), a newly discovered proinflammatory member of the IL-1 superfamily, may mediate this injury, but its role in the injured heart is currently not known. We first demonstrated the presence of IL-36(α/β) and its receptor (IL-36R) in ischemia/reperfusion-injured (IR-injured) mouse hearts and, interestingly, noted that expression of both increased with aging. An intravital model for imaging the adult and aged IR-injured beating heart in real time in vivo was used to demonstrate heightened basal and injury-induced neutrophil recruitment, and poorer blood flow, in the aged coronary microcirculation when compared with adult hearts. An IL-36R antagonist (IL-36Ra) decreased neutrophil recruitment, improved blood flow, and reduced infarct size in both adult and aged mice. This may be mechanistically explained by attenuated endothelial oxidative damage and VCAM-1 expression in IL-36Ra-treated mice. Our findings of an enhanced age-related coronary microcirculatory dysfunction in reperfused hearts may explain the poorer outcomes in elderly patients following MI. Since targeting the IL-36/IL-36R pathway was vasculoprotective in aged hearts, it may potentially be a therapy for treating MI in the elderly population.
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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.