通讯作者: 刘 悦

DOI：10.12201/bmr.202508.00029

Based on the theory of spleen as cardinal, the role of mitophagy mediating macrophage pyroptosis in atherosclerosis was discussed

• 摘要：动脉粥样硬化(AS)是动脉壁的一种慢性炎症性疾病。现代医学认为巨噬细胞稳态失衡,线粒体自噬功能减弱,诱导巨噬细胞焦亡,进而释放大量炎症因子造成AS。炎症反应可视为“痰、瘀”的微观表象。脾居中焦,为气机升降之枢纽。中医认为脾脏枢机失衡、气机失调,人体平衡破坏,气血津液输布障碍,痰瘀内生壅塞脉道,是其关键病机。线粒体是细胞内主要能量来源,是中医学理论中“脾”的现代生物学基础。因此本文认为线粒体自噬介导的巨噬细胞焦亡可能是“脾枢机失衡、痰瘀内生”的微观体现。故本文旨在“脾为枢机”理论指导下探讨线粒体自噬诱导巨噬细胞焦亡的病理机制,丰富“脾为枢机”内涵,为AS的诊疗提供理论依据。

  关键词： 脾脏; 枢机; 动脉粥样硬化; 线粒体自噬; 巨噬细胞焦亡

   

  Abstract: Atherosclerosis (AS) is a chronic inflammatory disease of the artery wall. Modern medicine believes that macrophage homeostasis is out of balance, mitochondrial autophagy function is weakened, and macrophage pyroptosis is induced, and then a large number of inflammatory factors are released to cause AS. The inflammatory response can be seen as a microscopic manifestation of phlegm and stasis. The spleen is in the middle of the coke, which is the hub of the lifting of the gas engine. Traditional Chinese medicine believes that the imbalance of the spleen cardinal, the imbalance of qi and organs, the destruction of the balance of the human body, the imbalance of qi, blood and fluid, and the internal obstruction of the veins by phlegm and stasis are the key pathogenesis. Mitochondria are the main source of energy in the cell, and they are the modern biological basis of the spleen in traditional Chinese medicine. Therefore, this paper suggests that mitochondrial autophagy-mediated pyroptosis of macrophages may be a microscopic manifestation of spleen cardinal imbalance and endophytic phlegm stasis. Therefore, the purpose of this paper is to explore the pathological mechanism of mitophagy autophagy-induced pyroptosis in macrophages under the guidance of the theory of spleen as cardinal, enrich the connotation of spleen as cardinal, and provide a theoretical basis for the diagnosis and treatment of AS.

  Key words: spleen; pivot; atherosclerosis; mitophagy; macrophages are pyroptosis

  提交时间：2025-08-12

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• 序号	提交日期	编号	操作
  1	2025-06-24	bmr.202508.00029V1	下载

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