Redox biology in pulmonary arterial hypertension (2013 Grover Conference Series).
Ontology highlight
ABSTRACT: Through detailed interrogation of the molecular pathways that contribute to the development of pulmonary arterial hypertension (PAH), the separate but related processes of oxidative stress and cellular metabolic dysfunction have emerged as being critical pathogenic mechanisms that are as yet relatively untargeted therapeutically. In this review, we have attempted to summarize some of the important existing studies, to point out areas of overlap between oxidative stress and metabolic dysfunction, and to do so under the unifying heading of redox biology. We discuss the importance of precision in assessing oxidant signaling versus oxidant injury and why this distinction matters. We endeavor to advance the discussion of carbon-substrate metabolism beyond a focus on glucose and its fate in the
SUBMITTER: Fessel JP
PROVIDER: S-EPMC4671734 | biostudies-literature | 2015 Dec
REPOSITORIES: biostudies-literature
ACCESS DATA