Interleukin-1β in Multifactorial Hypertension: Inflammation, Vascular Smooth Muscle Cell and Extracellular Matrix Remodeling, and Non-Coding RNA Regulation

Abstract

The biological activities of interleukins, a group of circulating cytokines, are linked to the immuno-pathways involved in many diseases. Mounting evidence suggests that interleukin-1β (IL-1β) plays a significant role in the pathogenesis of various types of hypertension. In this review, we summarized recent findings linking IL-1β to systemic arterial hypertension, pulmonary hypertension, and gestational hypertension. We also outlined the new progress in elucidating the potential mechanisms of IL-1β in hypertension, focusing on it's regulation in inflammation, vascular smooth muscle cell function, and extracellular remodeling. In addition, we reviewed recent studies that highlight novel findings examining the function of non-coding RNAs in regulating the activity of IL-1β and its associated proteins in the setting of hypertension. The information collected in this review provides new insights into understanding the pathogenesis of hypertension and could lead to the discovery of new anti-hypertensive therapies to combat this highly prevalent disease.

Keywords: IL-1β; hypertension; inflammation; interleukins; non-coding RNA; vascular smooth muscle cell.

Figure 1

Non-coding RNA regulation of IL-1β and its associated signaling in various hypertension conditions. Several ncRNAs function to block the pro-inflammatory actions of IL-1β in the setting of systemic hypertension, pulmonary hypertension, and gestational hypertension. IL-1β also inhibits miR-25 and is subsequently involved in the regulation of blood pressure. NLRP3: NLR family pyrin domain containing 3; ETRA: endothelin A receptor; KLF4: Kruppel like factor 4; HIF1: Hypoxia-inducible factors; ET1: Endothelin 1; CPS1-IT: CPS1 Intronic Transcript 1; MALAT 1: metastasis-associated lung adenocarcinoma transcript 1; VSMC: vascular smooth muscle cell.