Fig. 1.

Detrimental roles of selected adipokines in pulmonary hypertension A-H. Detrimental roles and underlying mechanisms of Leptin (A), Resistin (B), NAMPT (C), Chemerin (D), Lipocalin 2 (E), Gremlin-1 (F), DPP-4 (G) and SPARC (H) in the pathogenesis of pulmonary hypertension. I. Selected adipokines play detrimental roles in the pulmonary vascular remodeling of pulmonary hypertension. Abbreviation: BMP, bone morphogenetic protein; CaSR, calcium-sensing receptor; CMKRL1, chemerin chemokine-like receptor 1; DPP-4, dipeptidyl peptidase-4; ERK1/2, extracellular signal-regulated protein kinase 1/2; EndMT, endothelial to mesenchymal transition. ER stress, endoplasmic reticulum stress; GLP-1, glucagon-like peptide 1, HMGB1, high mobility group box 1; HIF-1, hypoxia inducible factor-1; MAPK, mitogen-activated protein kinase; NAMPT, nicotinamide phosphoribosyltansferase; PASMC, pulmonary artery smooth muscle cell; PAEC, pulmonary arterial endothelial cell; PPAR, peroxisome proliferation-activator receptor; PI3K, phosphatidylinositol 3 kinase; ROS, reactive oxygen species; SOD1/2, superoxide dismutases 1/2; SPARC, secreted protein acidic and rich in cysteine. STAT3, signal transduce and activator of transcription 3; Treg, regulatory T cell (Figures are created using Biorender. com).