| Literature DB >> 30080181 |
Miranda K Culley1, Stephen Y Chan1,2.
Abstract
Pulmonary hypertension (PH) is a heterogeneous and fatal disease of the lung vasculature, where metabolic and mitochondrial dysfunction may drive pathogenesis. Similar to the Warburg effect in cancer, a shift from mitochondrial oxidation to glycolysis occurs in diseased pulmonary vessels and the right ventricle. However, appreciation of metabolic events in PH beyond the Warburg effect is only just emerging. This Review discusses molecular, translational, and clinical concepts centered on the mitochondria and highlights promising, controversial, and challenging areas of investigation. If we can move beyond the "mountains" of obstacles in this field and elucidate these fundamental tenets of pulmonary vascular metabolism, such work has the potential to usher in much-needed diagnostic and therapeutic approaches for the mitochondrial and metabolic management of PH.Entities:
Mesh:
Substances:
Year: 2018 PMID: 30080181 PMCID: PMC6118596 DOI: 10.1172/JCI120847
Source DB: PubMed Journal: J Clin Invest ISSN: 0021-9738 Impact factor: 14.808