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. 2018 Jul 1;198(1):13–23. doi: 10.1164/rccm.201801-0062UP

Figure 1.

Figure 1.

Novel molecular and cellular insights into pulmonary arterial hypertension signaling reveals convergence of sex hormone, glucose metabolism, and inflammatory signaling on common effectors of the BMP (bone morphogenetic protein)/TGF-β (transforming growth factor) and PPAR-γ (peroxisome proliferator-activated receptor-γ) axes and other signaling axes. The yellow numbers indicate references. Illustration by Jacqueline Schaffer. 16α-OHE1 = 16α hydroxyestrone 1; ADAM = a disintegrin and metalloprotease; ALK = activin-like kinase; BMPR2 = BMP receptor type 2; DHEA = dehydroepiandrosterone; DHEA-S = dehydroepiandrosterone sulfate; ERα = estrogen receptor α; Fc = fragment crystallizable region; FK506 = tacrolimus; FKBP12 = FK506 binding protein; miR = microRNA; PAEC = pulmonary artery endothelial cell; PASMC = pulmonary artery smooth muscle cell; p-SMAD = phosphorylated SMAD; SMAD = fusion of Caenorhabditis elegans Sma genes and the Drosophila Mad, Mothers against decapentaplegic; SMURF1 = E3 ubiquitin-protein ligase SMURF1; TAZ = transcriptional co-activator with PDZ-binding motif; TGF-β1 = transforming growth factor β-1; TGF-β1R = TGF-β1 receptor; TNFα = tumor necrosis factor α; VEGFR3 = vascular endothelial growth factor receptor 3; YAP = Yes-8 associated protein.