Higaki Akinori, Mahmoud Ahmad U M, Paradis Pierre, Schiffrin Ernesto L
Lady Davis Institute for Medical Research.
Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, 3755 Côte-Ste-Catherine Road, Montreal, Quebec H3T 1E2, Canada.
Cardiovasc Res. 2021 Apr 23;117(5):1274-1283. doi: 10.1093/cvr/cvaa257.
Current knowledge suggests that hypertension is in part mediated by immune mechanisms. Both interleukin (IL)-23 and IL-17 are up-regulated in several experimental hypertensive rodent models, as well as in hypertensive humans in observational studies. Recent preclinical studies have shown that either IL-23 or IL-17A treatment induce blood pressure elevation. However, the IL-23/IL-17 axis has not been a major therapeutic target in hypertension, unlike in other autoimmune diseases. In this review, we summarize current knowledge on the role of these cytokines in immune mechanisms contributing to hypertension, and discuss the potential of IL-23/IL-17-targeted therapy for treatment of hypertension.
目前的知识表明,高血压部分由免疫机制介导。在几种实验性高血压啮齿动物模型以及观察性研究中的高血压患者体内,白细胞介素(IL)-23和IL-17均上调。最近的临床前研究表明,单独给予IL-23或IL-17A治疗均可导致血压升高。然而,与其他自身免疫性疾病不同,IL-23/IL-17轴尚未成为高血压的主要治疗靶点。在本综述中,我们总结了关于这些细胞因子在导致高血压的免疫机制中的作用的现有知识,并讨论了针对IL-23/IL-17的疗法治疗高血压的潜力。