肥胖相关性肝肾疾病的新机制

Mechanisms linking obesity,chronic kidney disease and fatty liver disease

肥胖是肥胖相关性肾病和非酒精性脂肪肝病的重要危险因素。近年来研究表明,组织内的血清胎球蛋白A和脂联素,以及5'-AMP激活的蛋白激酶(AMPK)的协同作用是肥胖相关性肝肾疾病的共同机制,在肾脏足细胞和肝实质细胞的损伤中发挥枢纽作用,引发组织炎症、纤维化,以及终末期硬化。深入研究该早期共同通路,有助于发现肥胖相关性疾病治疗的新靶标。

Obesity is a risk factor for chronic kidney disease and nonalcoholic fatty liver disease. Recent studies identify mechanisms common to both disease linked through an interorgan communication orchestrated by Fetuin-A, Adiponectin and 5＇-AMP activated protein kinase （AMPK）. In liver and kidney, the energy sensor 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 common sequelae of obesity.