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. 2023 Nov 17;9(11):e22482. doi: 10.1016/j.heliyon.2023.e22482

Fig. 2.

Fig. 2

Beneficial roles of selected adipokines in pulmonary hypertension A-G. Detrimental roles and underlying mechanisms of Adiponectin (A), CTRP9 (B), FGF21 (C), Apelin (D), Omentin-1 (E), FSTL1 (F) and Vaspin (G) in the pathogenesis of pulmonary hypertension. H. Selected adipokines play detrimental roles in the pulmonary vascular remodeling of pulmonary hypertension. Abbreviation: AMPK, 5′-adenosine monophosphate-activated protein kinase; APJ, apelin receptor; CTRP9, C1q/TNF-related protein 9; eNOS, endothelial nitric oxide synthase; EIF4EBP1, eukaryotic translation initiation Factor 4E–binding protein 1; ER stress, endoplasmic reticulum stress; ERK1/2, extracellular signal-regulated protein kinase 1/2; ET-1, endothelin-1; mTORC, mechanistic target of rapamycin complex 1; FGF21; fibroblast growth factor 21; FGFR1, fibroblast growth factor receptor 1; FSTL1, follistatin-like 1; KLF2, krupple-like factor 2; MMP-2, matrix metalloproteinas-2; PASMC, pulmonary artery smooth muscle cell; PAEC, pulmonary arterial endothelial cell; PPARγ, peroxisome proliferation-activator receptor γ; PGC-1α, PPARγ coactivator--1α; PI3K, phosphatidylinositol 3 kinase; SRF, serum response factor; TGF-1, transforming growth factor 1; ROS, reactive oxygen species (Figures are created using BioRender.com).