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- W2027858224 abstract "The receptor for advanced glycation end products (RAGE) is expressed in the heart in cardiomyocytes, vascular cells, fibroblasts, and in infiltrating inflammatory cells. Experiments in murine, rat, and swine models of injury suggest that RAGE and the ligands of RAGE are upregulated in key injuries to the heart, including ischemia/reperfusion injury, diabetes, and inflammation. Pharmacological antagonism of RAGE or genetic deletion of the receptor in mice is strikingly protective in models of these stresses. Data emerging from human studies suggest that measurement of levels of RAGE ligands or soluble RAGEs in plasma or serum may correlate with the degree of heart failure. Taken together, the ligand-RAGE axis is implicated in heart failure and we predict that therapeutic antagonism of RAGE might be a unique target for therapeutic intervention in this disorder." @default.
- W2027858224 created "2016-06-24" @default.
- W2027858224 creator A5007603996 @default.
- W2027858224 creator A5051573119 @default.
- W2027858224 date "2012-03-29" @default.
- W2027858224 modified "2023-10-02" @default.
- W2027858224 title "Receptor for Advanced Glycation End Products (RAGE) and Implications for the Pathophysiology of Heart Failure" @default.
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- W2027858224 doi "https://doi.org/10.1007/s11897-012-0089-5" @default.
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