Fig. 3
From: Novel insights and new therapeutic potentials for macrophages in pulmonary hypertension
The interaction between macrophages and other vessel cells in PH pathogenesis. Although macrophages might accelerate PH progression, pulmonary artery remodelling still results from abnormal angiogenesis. VECs, VSMCs and fibroblasts induce the recruitment of macrophages upon injury, while activated macrophages release variable mediators at different stages of inflammation. Influenced by these inflammatory mediators, vessel cells alter to specific phenotypes for survival or proliferation and release specific factors, such as IL-1, TGF-β, PDGF, or chemokines. These factors can regulate macrophage function and polarization in turn. For example, TGF-β contributes to M2-like polarization, while HMGB1 contributes to M1-like polarization. Together, these complex interactions eventually result in vascular remodelling and pulmonary hypertension