Lipodystrophy-Linked LMNA p.R482W Mutation Induces Clinical Early Atherosclerosis and In Vitro Endothelial Dysfunction | Zendy

Guillaume Bidault | Zendy; M. Garcia | Zendy; Marie-Christine Vantyghem | Zendy; Pierre-Henri Ducluzeau | Zendy; Romain Morichon | Zendy; K. Thiyagarajah | Zendy; Sylviane Moritz | Zendy; Jacqueline Capeau | Zendy; Corinne Vigouroux | Zendy; Véronique Béréziat | Zendy

Open Access

Lipodystrophy-Linked LMNA p.R482W Mutation Induces Clinical Early Atherosclerosis and In Vitro Endothelial Dysfunction

Author(s) -

Guillaume Bidault,

M. Garcia,

Marie-Christine Vantyghem,

Pierre-Henri Ducluzeau,

Romain Morichon,

K. Thiyagarajah,

Sylviane Moritz,

Jacqueline Capeau,

Corinne Vigouroux,

Véronique Béréziat

Publication year - 2013

Publication title -

arteriosclerosis, thrombosis, and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.113.301933

Subject(s) - lmna , lamin , medicine , endocrinology , biology , endothelial stem cell , phenotype , cancer research , endothelial dysfunction , genetics , in vitro , gene

Some mutations in LMNA, encoding A-type lamins, are responsible for Dunnigan-type-familial partial lipodystrophy (FPLD2), with altered fat distribution and metabolism. The high prevalence of early and severe cardiovascular outcomes in these patients suggests that, in addition to metabolic risk factors, FPLD2-associated LMNA mutations could have a direct role on the vascular wall cells.

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