Format

Send to

Choose Destination
Cell Metab. 2014 Apr 1;19(4):558-73. doi: 10.1016/j.cmet.2014.01.004. Epub 2014 Feb 6.

The metabolic basis of pulmonary arterial hypertension.

Author information

1
Department of Medicine, University of Alberta, 2C2 Walter Mackenzie Centre, 8440 112 Street Northwest, Edmonton, AB T6G 2P4, Canada.
2
Department of Medicine, University of Alberta, 2C2 Walter Mackenzie Centre, 8440 112 Street Northwest, Edmonton, AB T6G 2P4, Canada. Electronic address: em2@ualberta.ca.

Abstract

Pulmonary arterial hypertension (PAH) is a vascular remodeling disease of the lungs resulting in heart failure and premature death. Although, until recently, it was thought that PAH pathology is restricted to pulmonary arteries, several extrapulmonary organs are also affected. The realization that these tissues share a common metabolic abnormality (i.e., suppression of mitochondrial glucose oxidation and increased glycolysis) is important for our understanding of PAH, if not a paradigm shift. Here, we discuss an emerging metabolic theory, which proposes that PAH should be viewed as a syndrome involving many organs sharing a mitochondrial abnormality and explains many PAH features and provides novel biomarkers and therapeutic targets.

PMID:
24508506
DOI:
10.1016/j.cmet.2014.01.004
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center