Mitochondrial Dysfunction: Metabolic Drivers of Pulmonary Hypertension.

Journal Article (Journal Article;Review)

Significance: Pulmonary hypertension (PH) is a progressive disease characterized by pulmonary vascular remodeling and lung vasculopathy. The disease displays progressive dyspnea, pulmonary artery uncoupling and right ventricular (RV) dysfunction. The overall survival rate is ranging from 28-72%. Recent Advances: The molecular events that promote the development of PH are complex and incompletely understood. Metabolic impairment has been proposed to contribute to the pathophysiology of PH with evidence for mitochondrial dysfunction involving the electron transport chain proteins, antioxidant enzymes, apoptosis regulators, and mitochondrial quality control. Critical Issues: It is vital to characterize the mechanisms by which mitochondrial dysfunction contribute to PH pathogenesis. This review focuses on the currently available publications that supports mitochondrial mechanisms in PH pathophysiology. Future Directions: Further studies of these metabolic mitochondrial alterations in PH could be viable targets of diagnostic and therapeutic intervention.

Full Text

Duke Authors

Cited Authors

  • Suliman, HB; Nozik-Grayck, E

Published Date

  • October 20, 2019

Published In

Volume / Issue

  • 31 / 12

Start / End Page

  • 843 - 857

PubMed ID

  • 30604624

Pubmed Central ID

  • PMC6751393

Electronic International Standard Serial Number (EISSN)

  • 1557-7716

Digital Object Identifier (DOI)

  • 10.1089/ars.2018.7705


  • eng

Conference Location

  • United States