中国中医基础医学杂志2026，Vol.32Issue(9)：1859-1864,6.
基于"虚-瘀-毒"理论与线粒体内共生关系紊乱探讨动脉粥样硬化易损斑块的病机
Pathogenesis of Atherosclerotic Vulnerable Plaques Based on"Deficiency-Stasis-Toxin"Theory and Mitochondrial Endosymbiosis Disorder
摘要
Abstract
Atherosclerosis is a chronic inflammatory vascular disease affecting medium and large-sized arterial walls,with vulnerable plaque formation serving as the pathological basis for various thrombotic cardiovascular diseases.Dysregulation of mitochondrial endosymbiotic relationships can lead to structural and functional impairments of mitochondria,thereby interfering with signaling molecule release and triggering a series of pathological processes including inflammation,apoptosis,and oxidative stress,which exacerbate the progression of atherosclerotic vulnerable plaques.Based on the"deficiency-stasis-toxin"theory,this study identifies"deficiency of vital Qi"as the initiating factor for atherosclerotic plaque formation,"blood stasis and internal obstruction"as the pathological pivot,and"stasis-toxin interaction"as the key determinant of plaque vulnerability.Traditional Chinese medicine can regulate mitochondrial function through multi-target interventions such as replenishing Qi and strengthening vital Qi,promoting blood circulation to resolve stasis,and detoxifying to dissipate accumulation,thereby restoring endosymbiotic homeostasis.By exploring the intrinsic relationship between mitochondrial endosymbiotic dysregulation and"deficiency-stasis-toxin"pathogenesis,this study provides a modern biological interpretation of traditional Chinese medical theory and offers novel perspectives and strategies for clinical management of atherosclerotic vulnerable plaques.关键词
线粒体/内共生关系/虚瘀毒/动脉粥样硬化/易损斑块Key words
Mitochondria/Endosymbiosis/Deficiency-stasis-toxin/Atherosclerosis/Vulnerable plaque分类
医药卫生引用本文复制引用
李德秀,郑莉莹,薛梅,赵麟..基于"虚-瘀-毒"理论与线粒体内共生关系紊乱探讨动脉粥样硬化易损斑块的病机[J].中国中医基础医学杂志,2026,32(9):1859-1864,6.基金项目
国家自然科学基金面上项目(81973686) （81973686）
国家重点研发计划项目(2019YFC0840608) （2019YFC0840608）
中国中医科学院西苑医院能力提升项目(XYZX0201-18,XYZX0301-04) （XYZX0201-18,XYZX0301-04）
