Mitochondria: Roles in pulmonary hypertension

• Published in: The international journal of biochemistry & cell biology Vol. 55; pp. 93 - 97
• Main Authors: Freund-Michel, Véronique, Khoyrattee, Nafiisha, Savineau, Jean-Pierre, Muller, Bernard, Guibert, Christelle
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ltd 01.10.2014; Elsevier
• Subjects: Alterations; Animals; Arteries; Failure; Glycolysis; Human health and pathology; Humans; Hypertension; Hypertrophy, Right Ventricular - metabolism; Life Sciences; Mitochondria; Mitochondria - metabolism; Mitochondrial dysfunction; Models, Biological; Oxidation-Reduction; Oxidative Phosphorylation; Phosphorylation; Pulmonary arterial remodelling; Pulmonary Artery - metabolism; Pulmonary hypertension; Pulmonology and respiratory tract; Reactive Oxygen Species - metabolism; Right ventricular hypertrophy; Signalling; Right ventricular hypertrophy; Mitochondria; Mitochondrial dysfunction; Pulmonary arterial remodelling; Pulmonary hypertension
• ISSN: 1357-2725; 1878-5875
• DOI: 10.1016/j.biocel.2014.08.012

Mitochondria are essential cell organelles responsible for ATP production in the presence of oxygen. In the pulmonary vasculature, mitochondria contribute to physiological intracellular signalling pathways through production of reactive oxygen species and play the role of oxygen sensors that coordinate hypoxic pulmonary vasoconstriction. Mitochondria also play a pathophysiological role in pulmonary hypertension (PH). This disease is characterized by increased pulmonary arterial pressure and remodelling of pulmonary arteries, leading to increased pulmonary vascular resistance, hypertrophy of the right ventricle, right heart failure and ultimately death. Mitochondrial alterations have been evidenced in PH in pulmonary arteries and in the right ventricle, in particular a chronic shift in energy production from mitochondrial oxidative phosphorylation to glycolysis. This shift, initially described in cancer cells, may play a central role in PH pathogenesis. Further studies of these metabolic mitochondrial alterations in PH may therefore open new therapeutic perspectives in this disease.