MicroRNA-155 at the crossroads of inflammation and vascular dysfunction in essential hypertension.

MicroRNA-155 (miR-155) has emerged as a pivotal regulator in the development of hypertension. However, its role in the mechanism underlying hypertension remains incompletely defined, especially in vascular inflammation and dysfunction. This review synthesizes and evaluates the published literature on the role of miR-155 in the regulation of inflammation, endothelial dysfunction (ED), and vascular smooth muscle cells (VSMCs) function in essential hypertension (EH). We evaluated experimental and clinical studies investigating the expression patterns, molecular targets, and pathways involving miR-155 in endothelial cells (EC), VSMCs in hypertensive conditions. MiR-155 is consistently upregulated in the circulating and tissue of hypertensive models and patients. MiR-155 intensifies inflammation by suppressing endothelial nitric oxide synthase (eNOS) production, enhancing nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, and promoting pro-inflammatory cytokine expression. In EC, miR-155 directly targets eNOS, leading to impaired nitric oxide (NO) bioavailability and vasodilation by inhibiting the phosphatidylinositol-3-kinase/serine/threonine kinase (PI3K/Akt) pathway. miR-155 modulates the renin-angiotensin-aldosterone system (RAAS) by directly targeting angiotensin II Type 1 receptor (AT1R) mRNA, reducing its expression and attenuating angiotensin II (Ang II) signaling. In VSMCs, it promotes phenotypic switching and contributes to vascular remodeling through the soluble guanylate cyclase/cyclic guanosine monophosphate (sGC/cGMP) pathway. These coordinated actions foster a pro-inflammatory, vasoconstrictive state that underpins hypertension development. MiR-155 acts as a central molecular link between inflammation and vascular dysfunction in essential hypertension by modulating endothelial function, vascular inflammation, and smooth muscle cell behavior. Its modulation highlights miR-155 as a potential therapeutic target to restore endothelial homeostasis and limit vascular damage in hypertensive patients.