Targeting Energetic Metabolism A New Frontier in the Pathogenesis and Treatment of Pulmonary Hypertension

This perspective highlights advances in the understanding of the role of cellular metabolism in the pathogenesis of pulmonary hypertension. Insights gained in the past 20 years have revealed several similarities between the cellular processes underlying the pulmonary vascular remodeling in pulmonary...

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Bibliographic Details
Published in:American journal of respiratory and critical care medicine 2012-02, Vol.185 (3), p.260-266
Main Authors: TUDER, Rubin M, DAVIS, Laura A, GRAHAM, Brian B
Format: Article
Language:English
Subjects:
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Angiogenesis
Apoptosis
Apoptosis - physiology
Biological and medical sciences
Cancer
Cell cycle
Cell growth
Energy Metabolism - physiology
Glucose
Glycolysis - physiology
Growth factors
Humans
Hypertension, Pulmonary - diagnosis
Hypertension, Pulmonary - etiology
Hypertension, Pulmonary - therapy
Hypertrophy, Right Ventricular - etiology
Hypotheses
Hypoxia
Hypoxia-Inducible Factor 1 - antagonists & inhibitors
Hypoxia-Inducible Factor 1 - metabolism
Intensive care medicine
Intubation
Medical sciences
Metabolism
Mitochondria - physiology
Mutation
Oxidation
Pathogenesis
Phosphorylation
Pneumology
Pulmonary
Pulmonary arteries
Pulmonary hypertension
Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases
Veins & arteries
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Summary:This perspective highlights advances in the understanding of the role of cellular metabolism in the pathogenesis of pulmonary hypertension. Insights gained in the past 20 years have revealed several similarities between the cellular processes underlying the pulmonary vascular remodeling in pulmonary hypertension and those seen in cancer processes. In line with these insights, there is increasing recognition that abnormal cellular metabolism, notably of aerobic glycolysis (the "Warburg effect"), the potential involvement of hypoxia-inducible factor in this process, and alterations in mitochondrial function, are key elements in the pathogenesis of this disease. The glycolytic shift may underlie the resistance to apoptosis and increased vascular cell proliferation, which are hallmarks of pulmonary hypertension. These investigations have led to novel approaches in the diagnosis and therapy of pulmonary hypertension.
ISSN:1073-449X
1535-4970
DOI:10.1164/rccm.201108-1536PP