Overview of the dysfunctional metabolic pathways in pulmonary vascular cell types implicated in the development of pulmonary hypertension. Overview of.

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Overview of the dysfunctional metabolic pathways in pulmonary vascular cell types implicated in the development of pulmonary hypertension. Overview of the dysfunctional metabolic pathways in pulmonary vascular cell types implicated in the development of pulmonary hypertension. KG: ketoglutarate; ΔΨm: mitochondrial membrane potential; AMPK: adenosine monophosphate-activated protein kinase; ATF: activating transcription factor; Ca2+: calcium; DRP: dynamin-related protein; ER: endoplasmic reticulum; ETC: electron transport chain; FAO: fatty acid oxidation; Fe: iron; S: sulfur; Gln: glutamine; GLS1: glutaminase; Glu: glutamate; HIF: hypoxia-inducible factor; IDH: isocitrate dehydrogenase; Irp: iron-regulatory protein; ISCU: iron-sulfur cluster assembly protein; Kv1.2: voltage-dependent potassium channel 1.2; MCUC: mitochondrial calcium uniporter complex; miR-210: micro-RNA 210; Mit: mitochondria; MPTP: mitochondrial permeability transition pore; Nogo-B: neurite outgrowth inhibitor-B; O2: oxygen: PDH: pyruvate dehydrogenase; PDK: pyruvate dehydrogenase kinase; PFK: phosphofructokinase; PGC: proliferator-activated receptor-y coactivator; PHD: prolyl hydroxlase; ROS: reactive oxygen species; SERCA: sarco-/endoplasmic reticulum calcium-ATPase; TAZ: transcription coactivator with a PDZ-binding motif; TCA: tricarboxylic acid; UCP: uncoupling protein; YAP: yes-associated protein. Stephen Y. Chan, and Lewis J. Rubin Eur Respir Rev 2017;26:170094 ©2017 by European Respiratory Society