Molecular mechanisms of immune response regulating hypertensive inflammatory microenvironment

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.