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首页> 外文期刊>Journal of the American Society of Nephrology: JASN >Mechanisms linking obesity, chronic kidney disease, and fatty liver disease: the roles of fetuin-A, adiponectin, and AMPK.
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Mechanisms linking obesity, chronic kidney disease, and fatty liver disease: the roles of fetuin-A, adiponectin, and AMPK.

机译:肥胖,慢性肾脏疾病和脂肪肝疾病的关联机制:胎球蛋白A,脂联素和AMPK的作用。

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摘要

Obesity is a risk factor for chronic kidney disease (CKD) and nonalcoholic fatty liver disease (NAFLD). Recent studies identify mechanisms common to both diseases linked through an interorgan communication orchestrated by fetuin-A and adiponectin. In liver and kidney, the energy sensor 5'-AMP activated protein kinase (AMPK) is pivotal to directing podocytes and hepatocytes to compensatory and potentially deleterious pathways, leading to inflammatory and profibrotic cascades culminating in end-organ damage. Regulation of these early upstream pathways may provide new therapeutic targets for these increasingly common sequelae of obesity.
机译:肥胖是慢性肾脏疾病(CKD)和非酒精性脂肪肝疾病(NAFLD)的危险因素。最近的研究确定了两种疾病的共同机制,这两种机制是通过胎球蛋白A和脂联素精心策划的器官间通讯联系在一起的。在肝脏和肾脏中,能量传感器5'-AMP活化蛋白激酶(AMPK)对于指导足细胞和肝细胞进入补偿性途径和潜在的有害途径至关重要,从而导致炎症和纤维化级联反应最终导致终末器官损害。这些早期上游途径的调节可能为这些日益常见的肥胖后遗症提供新的治疗靶标。

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