靶向白介素-27治疗冠状动脉疾病的新进展

IF 2.4 3区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

Journal of Cardiovascular Translational Research Pub Date : 2025-07-07 DOI:10.1007/s12265-025-10656-5

Wei-Lin Liang, Liang Liu, Bo Liang

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引用次数: 0

摘要

冠状动脉疾病（CAD）越来越被认为是一种慢性炎症性疾病。白细胞介素-27 （IL-27）是一种来自IL-12和IL-6家族的细胞因子，在CAD发病中起双重作用。它通过与IL-1β相互作用并激活NLRP3炎性体，促进炎症和组织损伤，从而加剧疾病。相反，IL-27可以通过参与STAT1/3信号传导、抑制炎症和促进组织修复来延缓疾病进展。未来的研究应侧重于阐明IL-27的特异性生物学功能、与分子靶点的相互作用以及在CAD中的临床意义。这将增强对CAD的理解，并支持改进诊断和治疗策略的发展。

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Recent Insights Into Targeting Interleukin-27 in Coronary Artery Disease.

Coronary artery disease (CAD) is increasingly recognized as a chronic inflammatory condition. Interleukin-27 (IL-27), a cytokine from the IL-12 and IL-6 families, plays a dual role in CAD pathogenesis. It exacerbates disease by interacting with IL-1β and activating the NLRP3 inflammasome, promoting inflammation and tissue damage. Conversely, IL-27 can delay disease progression by engaging STAT1/3 signalling, suppressing inflammation, and promoting tissue repair. Future research should focus on elucidating IL-27's specific biological functions, interactions with molecular targets, and clinical implications in CAD. This will enhance understanding of CAD and support the development of improved diagnostic and therapeutic strategies.

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来源期刊

Journal of Cardiovascular Translational Research CARDIAC & CARDIOVASCULAR SYSTEMS-MEDICINE, RESEARCH & EXPERIMENTAL

CiteScore

6.10

自引率

2.90%

发文量

148

审稿时长

6-12 weeks

期刊介绍： Journal of Cardiovascular Translational Research (JCTR) is a premier journal in cardiovascular translational research. JCTR is the journal of choice for authors seeking the broadest audience for emerging technologies, therapies and diagnostics, pre-clinical research, and first-in-man clinical trials. JCTR''s intent is to provide a forum for critical evaluation of the novel cardiovascular science, to showcase important and clinically relevant aspects of the new research, as well as to discuss the impediments that may need to be overcome during the translation to patient care.