It is generally accepted that estrogens affect and modulate the development and progression of chronic kidney diseases (CKD) not related to diabetes. Clinical studies have indeed demonstrated that the severity and rate of progression of renal damage tends to be greater among men, compared with women. Experimental studies also support the notion that female sex is protective and male sex permissive, for the development of CKD in non-diabetics, through the opposing actions of estrogens and testosterone. However, when we consider diabetes-induced kidney damage, in the setting of either type 1 or type 2 diabetes, the contribution of gender to the progression of renal disease is somewhat uncertain. Previous studies on the effects of estrogens in the pathogenesis of progressive kidney damage have primarily focused on mesangial cells. More recently, data on the effects of estrogens on podocytes, the cell type whose role may include initiation of progressive diabetic renal disease, became available.
The aim of this review will be to summarize the main clinical and experimental data on the effects of estrogens on the progression of diabetes-induced kidney injury. In particular, we will highlight the possible biological effects of estrogens on podocytes, especially considering those critical for the pathogenesis of diabetic kidney damage.
Keywords: Estrogens, Chronic kidney disease, Diabetic kidney damage, Podocytes, Apoptosis, IgA neph-ropathy, polycystic kidney disease, testosterone, 17-estradiol (E2), glomerulosclerosis, ERKO, synthetic progestin, proteinuria, creatinine, medroxyprogesterone, tubulointerstitial, GS, TGF- synthesis, decreased, laminin, fibronectin, matrix metalloproteinases (MMPs), raloxifene, OLEFT, estrogen receptor (ER) subtypes, ER, p38 mitogen-activated protein kinase, TGF-1, vanced glycation end products, phosphoinositide 3-kinase (PI3K), AKT (protein kinase B), TNF, PI3K, respiratory chain (MRC), Mn-superoxide dismutase (MnSOD), glutathione (GSH), MMP-9 activity, HSP27, p38MAPK
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