Szrejder Maria, Piwkowska Agnieszka
Mossakowski Medical Research Centre Polish Academy of Sciences, Laboratory of Molecular and Cellular Nephrology, Gdańsk, Poland.
Biol Cell. 2019 May;111(5):109-120. doi: 10.1111/boc.201800077. Epub 2019 Feb 21.
Diabetic nephropathy is a major long-term complication of diabetes mellitus and one of the most common causes of end-stage renal disease. Thickening of the glomerular basement membrane, glomerular cell hypertrophy and podocyte loss are among the main pathological changes that occur during diabetic nephropathy, resulting in proteinuria. Injury to podocytes, which are a crucial component of the glomerular filtration barrier, seems to play a key role in the development of diabetic nephropathy. Recent studies have suggested that dysregulation of AMP-activated kinase protein, which is an essential cellular energy sensor, may play a fundamental role in this process. The purpose of this review is to highlight the molecular mechanisms associated with AMP-activated protein kinase (AMPK) in podocytes that are involved in the pathogenesis of diabetic nephropathy.
糖尿病肾病是糖尿病的一种主要长期并发症，也是终末期肾病最常见的病因之一。肾小球基底膜增厚、肾小球细胞肥大和足细胞丢失是糖尿病肾病发生过程中的主要病理变化，可导致蛋白尿。足细胞作为肾小球滤过屏障的关键组成部分，其损伤似乎在糖尿病肾病的发展中起关键作用。最近的研究表明，AMP激活的蛋白激酶（一种重要的细胞能量传感器）失调可能在此过程中起根本作用。本综述的目的是强调足细胞中与AMP激活的蛋白激酶（AMPK）相关的分子机制，这些机制参与了糖尿病肾病的发病过程。
