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Signaling of Serum Amyloid A Through Receptor for Advanced Glycation End Products as a Possible Mechanism for Uremia-Related Atherosclerosis
Author(s) -
Karim Belmokhtar,
Thomas Robert,
Jérémy Ortillon,
Antoine Braconnier,
Vincent Vuiblet,
Camille BoulagRombi,
Marie Danièle Diebold,
Christine Piètrement,
Ann Marie Schmidt,
Philippe Rieu,
Fatouma Touré
Publication year - 2016
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.115.306349
Subject(s) - glycation , uremia , mechanism (biology) , amyloid (mycology) , receptor , advanced glycation end product , medicine , chemistry , endocrinology , pathology , philosophy , epistemology
Cardiovascular disease is the leading cause of death in patients with end-stage renal disease. Serum amyloid A (SAA) is an acute phase protein and a binding partner for the multiligand receptor for advanced glycation end products (RAGE). We investigated the role of the interaction between SAA and RAGE in uremia-related atherogenesis.

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