Figure 5
From: Integrative proteomics and phosphoproteomics in pulmonary arterial hypertension
Dysregulated biological pathways and mitochondrial respiration in PAH. (a) Integrative analysis of proteomics and metabolomics reveals metabolic changes in PAH. Red arrow denotes elevated in PAH, and green arrow denotes decreased in PAH. Differentially expressed mitochondrial proteins by proteomics framed with black. Blue star, NAD+ is reduced to NADH. ADMA, asymmetric dimethylarginine; αKG, alpha-ketoglutarate; AKT1, RAC-alpha serine/threonine-protein kinase; ALDH18A1, delta-1-pyrroline-5-carboxylate synthase; ARG2, arginase 2; ETC, electron transport chain; fMet, N-formylmethionine; MTHFD1L, monofunctional C1-tetrahydrofolate (THF) synthase; NO, nitric oxide; NOS3, endothelial nitric oxide synthase; P5C, Δ1-pyrroline-5-carboxylate; SHMT2, serine hydroxymethyltransferase; SLC25A1, tricarboxylate transport protein; SOD1, superoxide dismutase [Cu-Zn]; TCA cycle, tricarboxylic acid cycle, THF, tetrahydrofolate. (b) Extracellular acidification rate (ECAR) vs. oxygen consumption rate (OCR) in PAH PAEC and healthy control PAEC. Mean of measurements are shown following addition of glucose at specified doses. PAH PAEC (n = 10) had a significant shift of the curve compared to control PAEC (n = 9) (P = 0.04).
