Munehiro Kitada1,2, Yoshio Ogura3, Itaru Monno3, Daisuke Koya3,4. 1. Department of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, Japan. kitta@kanazawa-med.ac.jp. 2. Division of Anticipatory Molecular Food Science and Technology, Medical Research Institute, Kanazawa Medical University, Uchinada, Ishikawa, Japan. kitta@kanazawa-med.ac.jp. 3. Department of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, Japan. 4. Division of Anticipatory Molecular Food Science and Technology, Medical Research Institute, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
Abstract
PURPOSE OF REVIEW: Autophagy promotes cellular health in response to various cellular stresses and to changes in nutrient conditions. In this review, we focus on the role of autophagy in the pathogenesis of diabetic nephropathy and discuss the regulation of autophagy as a new therapeutic target for the suppression of diabetic nephropathy. RECENT FINDINGS: Previous studies have indicated that autophagy deficiency or insufficiency in renal cells, including podocytes, mesangial cells, endothelial cells and tubular cells, contributes to the pathogenesis of diabetic nephropathy. Alterations in the nutrient-sensing pathways, including mammalian target of rapamycin complex1 (mTORC1), AMP-activated kinase (AMPK) and Sirt1, due to excess nutrition in diabetes are implicated in the impairment of autophagy. Maintaining both basal and adaptive autophagy against cellular stress may protect the kidney from diabetes-induced cellular stresses. Therefore, the activation of autophagy through the modulation of nutrient-sensing pathways may be a new therapeutic option for the suppression of diabetic nephropathy.
PURPOSE OF REVIEW: Autophagy promotes cellular health in response to various cellular stresses and to changes in nutrient conditions. In this review, we focus on the role of autophagy in the pathogenesis of diabetic nephropathy and discuss the regulation of autophagy as a new therapeutic target for the suppression of diabetic nephropathy. RECENT FINDINGS: Previous studies have indicated that autophagy deficiency or insufficiency in renal cells, including podocytes, mesangial cells, endothelial cells and tubular cells, contributes to the pathogenesis of diabetic nephropathy. Alterations in the nutrient-sensing pathways, including mammalian target of rapamycin complex1 (mTORC1), AMP-activated kinase (AMPK) and Sirt1, due to excess nutrition in diabetes are implicated in the impairment of autophagy. Maintaining both basal and adaptive autophagy against cellular stress may protect the kidney from diabetes-induced cellular stresses. Therefore, the activation of autophagy through the modulation of nutrient-sensing pathways may be a new therapeutic option for the suppression of diabetic nephropathy.
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