Key result
The metabolic theory of pulmonary hypertension proposes that aberrations in metabolism and mitochondrial function are a major underlying cause of the disease, offering new therapeutic targets.
Why the study?
The metabolic theory of pulmonary hypertension proposes metabolism and mitochondrial dysfunction as key causes, but the timing and extent of these changes remain unknown.
Answers are grounded in this paper and cite their sources.
This review highlights the emerging metabolic theory of pulmonary hypertension, suggesting that metabolic and mitochondrial aberrations may be a major underlying cause and a promising therapeutic target.
Pulmonary hypertension (PH) encompasses a group of progressive and incurable cardiopulmonary disorders characterized by pulmonary vascular remodeling and increased mean pulmonary artery pressure leading to right heart failure. Emerging data suggest a common etiology for the reported diverse molecular and physiological abnormalities observed in the pulmonary vasculature: the metabolic theory of PH. This theory proposes that aberrations in metabolism and mitochondrial function are a major underlying cause for the cellular and organ level PH phenotype. Additionally, the metabolic theory of PH provides a rationale for the observed metabolic defects in other organs and systems outside of the pulmonary vasculature, including the right ventricle (RV), immune system, and skeletal muscle. However, whether these metabolic changes are driving disease and the timing and extent of these aberrations are still unknown. This review highlights: 1) key examples of metabolic alterations in the pulmonary vasculature, RV, inflammatory cells, and skeletal muscle; 2) examples of promising therapeutic interventions directly modifying metabolism; and 3) key remaining questions about the role of metabolic remodeling in PH.
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Frump et al. (2018) conducted a review in Pulmonary Arterial Hypertension. The metabolic theory of pulmonary hypertension proposes that aberrations in metabolism and mitochondrial function are a major underlying cause of the disease, offering new therapeutic targets.
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