A clinical link between peroxisome proliferator-activated receptor γ and the renin-angiotensin system. Arterioscler Thromb Vasc Biol 2013 Apr;33(4):676-8
Date
03/15/2013Pubmed ID
23486770Pubmed Central ID
PMC3905617DOI
10.1161/ATVBAHA.112.301125Scopus ID
2-s2.0-84875340383 (requires institutional sign-in at Scopus site) 8 CitationsAbstract
A mechanistic link between PPARγ and the renin-angiotensin system (RAS) has been previously proposed but clinical evidence supporting the relationship is incomplete. In the current issue of Arteriosclerosis Thrombosis Vascular Biology, Caron-Debarle et al. show that four patients with familial partial lipodystrophy associated with early-onset severe hypertension (FPLD3) carry mutations in PPARγ that impair its ability to act as a ligand-activated transcription factor. Cells isolated from these patients, and cells transfected with the same mutations in PPARγ exhibit activation of the cellular RAS, increased production of reactive oxygen species and markers of inflammation, all of which are dependent upon the angiotensin-II AT1 receptor. This translational study further supports a role for PPARγ as a regulator of blood pressure through its ability to modulate the RAS.
Author List
Sigmund CDAuthor
Curt Sigmund PhD Chair, Professor in the Physiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsFemale
Humans
Hypertension
Lipodystrophy, Familial Partial
Male
Mutation
PPAR gamma
Renin-Angiotensin System
