首页|期刊导航|中国中医基础医学杂志|基于"瘀热毒"理论探讨cGAS/STING 通路调控心肌梗死的机制

基于"瘀热毒"理论探讨cGAS/STING 通路调控心肌梗死的机制OA

Exploring the Mechanism of Myocardial Infarction Regulated by the cGAS/STING Pathway Based on the"Stasis-Heat-Toxicity"Theory

中文摘要英文摘要

本文基于中医"瘀热毒"理论探讨环状鸟苷酸-腺苷酸合成酶(cGAS)/干扰素基因刺激因子(STING)信号通路在心肌梗死发病机制中的作用.中医认为"瘀热毒"是引发心肌梗死的关键病理机制之一,瘀血阻滞,郁热化毒,三者相互影响,互相转化,从而加剧病情恶化.cGAS/STING 通路通过调控 M1 型巨噬细胞极化介导炎症反应,在心肌梗死的发病过程中发挥重要作用,此与瘀、热、毒三种邪气的产生及动态演变密切相关,是瘀、热、毒的微观表现.清热活血解毒类中药可通过阻断 cGAS/STING 通路减轻炎症反应,抑制 M1 型巨噬细胞极化,改善心功能,减少梗死面积,是心肌梗死的潜在治疗靶点.

This study explores the role of the cGAS/STING pathway in the pathogenesis of myocardial Infarction(MI)based on the"stasis-heat-toxicity"theory in traditional Chinese medicine(TCM).TCM posits that"stasis-heat-toxicity"constitutes one of the key pathological factor triggering myocardial infarction.Blood stasis obstruction leads to stagnant heat transforming into toxins,with these three elements interacting through mutual promotion and transformation,thereby exacerbating disease progression.The cGAS/STING pathway plays a crucial role in the pathogenesis of myocardial infarction by modulating M1 macrophage polarization and mediating inflammatory responses.This mechanism closely aligns with the generation and dynamic transformation of stasis,heat,and toxicity,serving as their microscopic manifestation.Notably,TCM herbal interventions with heat-clearing,blood-activating,and toxin-resolving properties may attenuate inflammation by inhibiting the cGAS/STING pathway,suppress M1 macrophage polarization,improve cardiac function,and reduce Infarction size,thereby highlighting this pathway as a potential therapeutic target for MI.

陈梦婷;王栋;盛明;张鹏

湖北中医药大学第一临床学院,武汉 430061||武汉市中医医院,武汉 430014北京中医药大学东直门医院,北京 100700湖北中医药大学第一临床学院,武汉 430061||武汉市中医医院,武汉 430014湖北中医药大学第一临床学院,武汉 430061||武汉市中医医院,武汉 430014

医药卫生

瘀热毒心肌梗死cGAS/STING 通路免疫炎症反应

Stasis-heat-toxicityMyocardial infarctioncGAS/STING PathwayImmunityInflammatory response

《中国中医基础医学杂志》 2026 (6)

1210-1214,5

国家自然科学基金面上项目(82474331)中国博士后科学基金面上项目(2024M760286)湖北省中医药管理局中医药科研项目(ZY2025M036)

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