Journal
NATURE COMMUNICATIONS
Volume 3, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms2087
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Funding
- la Fondation pour la Recherche Medicale (FRM)
- centre national pour la recherche scientifique (CNRS)
- University of Strasbourg
- Fondation de France
- Agence Nationale de la Recherche [ANR-06-PHYSIO-032-01, ANR-09-BLAN-0121-01]
- National Institutes of Health
- American Health Assistance Foundation
- Perot Family Foundation
- Consortium for Frontotemporal Dementia Research (CFR)
- Wolfgang-Paul Program of the Humboldt Foundation
- Agence Nationale de la Recherche (ANR) [ANR-09-BLAN-0121] Funding Source: Agence Nationale de la Recherche (ANR)
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Vascular calcification is a hallmark of advanced atherosclerosis. Here we show that deletion of the nuclear receptor PPAR. in vascular smooth muscle cells of low density lipoprotein receptor (LDLr)-deficient mice fed an atherogenic diet high in cholesterol, accelerates vascular calcification with chondrogenic metaplasia within the lesions. Vascular calcification in the absence of PPAR. requires expression of the transmembrane receptor LDLr-related protein-1 in vascular smooth muscle cells. LDLr-related protein-1 promotes a previously unknown Wnt5a-dependent prochondrogenic pathway. We show that PPAR. protects against vascular calcification by inducing the expression of secreted frizzled-related protein-2, which functions as a Wnt5a antagonist. Targeting this signalling pathway may have clinical implications in the context of common complications of atherosclerosis, including coronary artery calcification and valvular sclerosis.
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