免疫应答调控高血压炎症微环境的分子机制

Molecular mechanisms of immune response regulating hypertensive inflammatory microenvironment

  • 摘要: 慢性低度炎症持续存在是高血压的关键驱动因素。补体分子与炎症因子紊乱损伤血管、神经-免疫细胞交互作用、免疫应答失调加剧靶器官炎症等分子机制协同打破高血压炎症微环境稳态。脑-肠轴机制是高血压炎症的新热点,肠道菌群通过短链脂肪酸/氧化三甲胺影响体内免疫应答,诱发炎症影响血压。文章通过整合多维度研究成果,论述高血压免疫方向的新研究、新进展及新靶点,为深入理解高血压的免疫调节提供了新的理论依据。

     

    Abstract: Persistence of chronic low-grade inflammation is a key driver of hypertension. Molecular mechanisms such as complement molecules and inflammatory factor disorders damaging blood vessels, neuro-immune cell interactions, and immune response dysregulation aggravating target organ inflammation synergistically break the homeostasis of the inflammatory microenvironment of hypertension. The brain-gut axis mechanism is a new hotspot of hypertension inflammation. Gut microbiota affects the immune response in vivo through short-chain fatty acids (SCFAs)/trimethylamine oxide (TMAO), inducing inflammation and affecting blood pressure. In this article, by integrating the results of multi-dimensional research, new research, new progress and new targets in the direction of hypertension immunity were discussed, providing a new theoretical basis for in-depth understanding of the immunoregulation of hypertension.

     

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