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. 2022 Mar 2;9:838657. doi: 10.3389/fcvm.2022.838657

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Copyright © 2022 Wang, Yan, Xu, Gong, Zhong, An, Zhao, Liu, Wang, Yuan and Jiang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Overview of glutamine metabolism in pulmonary arterial hypertension. Under pathological stress or upon activation of oncogenes, glutamine (Gln) is transported from extracellular to intracellular space by alanine-serine-cysteine transporter 2 (ASCT2) [also known as solute carrier family 1, member 5 (SLC1A5)]. Gln is then hydrolyzed to glutamate (GLU) and ammonia (NH3) driven by increased GLS expression in mitochondria. GLU is transformed into α-ketoglutaric acid (α-KG), which participates in the tricarboxylic acid (TCA) cycle for energy supply. During the process, the abnormal glutamine metabolism would ultimately lead to the pathological changes of pulmonary arterial hypertension via modulation of redox homeostasis, cell proliferation, autophagy and synthesis of biological macromolecules. Myc, MYC proto-oncogene; KRAS, kirsten rat sarcoma viral oncogene; p53, p53 gene; GLUD, glutamate dehydrogenase; ISO, isocitrate; Cit, citrate; OAA, oxaloacetate; Mal, malate; Fum, fumarase; Suc, succinic acid; Asn, asparagine; Asp, aspartate; ASL, argininosuccinate lyase; NO, nitric oxide; Pyr, pyruvate; NADPH, nicotinamide adenine dinucleotide phosphate; NADP, nicotinamide adenine dinucleotide phosphate.