Implication of advanced glycation end products (Ages) and their receptor (Rage) on myocardial contractile and mitochondrial functions.
Advanced glycation end products (AGEs) play an important role for the development and/or progression of cardiovascular diseases, mainly through induction of oxidative stress and inflammation. AGEs are a heterogeneous group of molecules formed by non-enzymatic reaction of reducing sugars with amino acids of proteins, lipids and nucleic acids. AGEs are mainly formed endogenously, while recent studies suggest that diet constitutes an important exogenous source of AGEs. The presence and accumulation of AGEs in various cardiac cell types affect extracellular and intracellular structure and function. AGEs contribute to a variety of microvascular and macrovascular complications through the formation of cross-links between molecules in the basement membrane of the extracellular matrix and by engaging the receptor for advanced glycation end products (RAGE). Activation of RAGE by AGEs causes up regulation of the transcription factor nuclear factor-κB and its target genes. of the RAGE engagement stimulates oxidative stress, evokes inflammatory and fibrotic reactions, which all contribute to the development and progression of devastating cardiovascular disorders. This review discusses potential targets of glycation in cardiac cells, and underlying mechanisms that lead to heart failure with special interest on AGE-induced mitochondrial dysfunction in the myocardium.
Department of Physiology, School of Medicine, Pole Recherche 1, place de Verdun, 59045, Lille Cedex, France. rneviere@univ-lille2.fr.|LIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France. rneviere@univ-lille2.fr.
Remi
R
Neviere
LIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France.|School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yichi
Y
Yu
LIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France.|School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Lei
L
Wang
LIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France.
Frederic
F
Tessier
LIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France.
Eric
E
Boulanger
D002318:Cardiovascular Diseases / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism* / Q000473:pathology; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress; D000067759:Receptor for Advanced Glycation End Products / Q000378:metabolism*
C000593871:AGER protein, human; D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products
Advanced glycation end products; Cardiovascular; Mitochondria; Signaling pathways