Zhang Haifeng, Huang Wenhui, Bao Shisan
Department of Cardiology, The First People's Hospital of Baiyin, Baiyin, Gansu, China.
Front Immunol. 2025 Jul 8;16:1642116. doi: 10.3389/fimmu.2025.1642116. eCollection 2025.
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.
白细胞介素-1（IL-1）超家族成员在协调炎症和免疫反应中发挥着关键作用。其中，IL-36和IL-38已成为在心血管疾病（CVD）中具有相反作用的细胞因子。IL-36通常促进炎症，导致内皮功能障碍、动脉粥样硬化和心肌损伤。相比之下，IL-38主要发挥抗炎作用，调节免疫反应并促进组织修复。本综述对目前关于IL-36和IL-38在动脉粥样硬化、心肌缺血再灌注（I/R）损伤以及经皮冠状动脉介入治疗（PCI）后结果方面的研究进行了批判性总结。我们讨论了它们的分子机制、作为生物标志物的潜力以及治疗意义，同时确定了值得进一步研究的关键知识空白。
