期刊
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
卷 309, 期 10, 页码 E807-E820出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00266.2015
关键词
diabetic nephropathy; diabetes mellitus; cell signaling; oxidative
资金
- National Institutes of Health, National Institute of Diabetes, Digestive and Kidney Diseases [RO1 DK-087707, RO1 DK-094987, RO1 DK-103694]
- Duke O'Brien Center for Kidney Research [P30 DK-096493]
- American Society of Nephrology Foundation for Kidney Research (Ben J. Lipps Research Fellowship)
- Edna and Fred L. Mandel, Jr. Center for Hypertension and Atherosclerosis research
Diabetic nephropathy (DN) is a serious complication of both type 1 and type 2 diabetes mellitus. The disease is now the most common cause of end-stage kidney disease (ESKD) in developed countries, and both the incidence and prevalence of diabetes mellitus is increasing worldwide. Current treatments are directed at controlling hyperglycemia and hypertension, as well as blockade of the renin angiotensin system with angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin receptor blockers. Despite these therapies, DN progresses to ESKD in many patients. As a result, much interest is focused on developing new therapies. It has been over two decades since ACEIs were shown to have beneficial effects in DN independent of their blood pressure-lowering actions. Since that time, our understanding of disease mechanisms in DN has evolved. In this review, we summarize major cell signaling pathways implicated in the pathogenesis of diabetic kidney disease, as well as emerging treatment strategies. The goal is to identify promising targets that might be translated into therapies for the treatment of patients with diabetic kidney disease.
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