Implication of advanced glycation end products (Ages) and their receptor (Rage) on myocardial contractile and mitochondrial functions
| Autor: | Yichi Yu, Remi Neviere, Lei Wang, Eric Boulanger, Frédéric J. Tessier |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Glycation End Products Advanced medicine.medical_specialty Receptor for Advanced Glycation End Products Inflammation 030204 cardiovascular system & hematology Mitochondrion Biology medicine.disease_cause Biochemistry Mitochondria Heart RAGE (receptor) 03 medical and health sciences 0302 clinical medicine Glycation Internal medicine Extracellular medicine Humans Receptor Molecular Biology Myocardium Cell Biology Myocardial Contraction Oxidative Stress 030104 developmental biology Endocrinology Cardiovascular Diseases medicine.symptom Signal transduction Oxidative stress |
| Zdroj: | Glycoconjugate journal. 33(4) |
| ISSN: | 1573-4986 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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