New Insights Into HIMF (Hypoxia-Induced Mitogenic Factor)-Mediated Signaling Pathways in Pulmonary Hypertension.

Abstract

Endothelial cell (EC) dysfunction, characterized by cell injury, ensuing apoptosis, and release of growth factors and cytokines, is a critical early event in the pathogenesis of many cardiovascular diseases, including pulmonary hypertension (PH). Indeed, excessive production of paracrine factors from damaged EC promotes the recruitment of circulating inflammatory cells and triggers vascular remodeling through stimulation of pulmonary artery (PA) smooth muscle cell (SMC) contraction and proliferation. Although endothelium injury is recognized to play a causative role in the development and progression of PH, the underlying mechanisms as well as the nature of the signaling molecules that mediates crosstalk between PAECs and adjacent SMCs remain poorly understood.