Key result
IL-36 drives inflammation and atherogenesis in CVD, whereas IL-38 promotes repair and suppresses inflammation.
Why the study?
IL-36 and IL-38 have contrasting roles in cardiovascular disease, but their molecular mechanisms, biomarker potential, and therapeutic implications require critical synthesis and further investigation.
IL-36 and IL-38 have contrasting pro- and anti-inflammatory roles in cardiovascular disease, presenting potential novel biomarkers and therapeutic targets.
Members of the interleukin-1 (IL-1) superfamily play crucial roles in orchestrating inflammation and immune responses. Among them, IL-36 and IL-38 have emerged as cytokines with contrasting roles in cardiovascular disease (CVD). IL-36 typically promotes inflammation, contributing to endothelial dysfunction, atherogenesis, and myocardial injury. In contrast, IL-38 exerts predominantly anti-inflammatory effects, modulating immune responses and promoting tissue repair. This mini-review provides a critical synthesis of current findings on IL-36 and IL-38 in the context of atherosclerosis, myocardial ischaemia-reperfusion (I/R) injury, and post-percutaneous coronary intervention (PCI) outcomes. We discuss their molecular mechanisms, potential as biomarkers, and therapeutic implications, while identifying key gaps in knowledge that merit further investigation.
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Zhang et al. (2025) conducted a review in Cardiovascular disease. IL-36 and IL-38 was evaluated. IL-36 promotes inflammation and atherogenesis in cardiovascular disease, whereas IL-38 exerts predominantly anti-inflammatory effects and promotes tissue repair.
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