Receptor for advanced glycation end products (RAGE) and implications for the pathophysiology of heart failure.
Receptor for advanced glycation end products (RAGE) and implications for the pathophysiology of heart failure.
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DOI：
10.1007/s11897-012-0089-5
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发表时间：
2012-06
影响因子：
--
通讯作者：
Schmidt AM
中科院分区：
文献类型：
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作者：
Ramasamy R;Schmidt AM
晚期糖基化终末产物受体（AGEs）在心脏的心肌细胞、血管细胞、成纤维细胞和浸润性炎症细胞中表达。在小鼠、大鼠和猪损伤模型中的实验表明，在心脏的关键损伤中，包括缺血/再灌注损伤、糖尿病和炎症，β-淀粉样蛋白和β-淀粉样蛋白配体上调。药理学拮抗作用的受体或基因缺失的小鼠是惊人的保护这些压力的模型。来自人类研究的数据表明，血浆或血清中的RAGE配体或可溶性RAGE水平的测量可能与心力衰竭的程度相关。两者合计，配体-受体轴与心力衰竭有关，我们预测受体轴的治疗性拮抗作用可能是这种疾病治疗干预的独特靶点。
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.