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1 osis (FSGS) and streptozotocin (STZ)-induced diabetic glomerulosclerosis.
2 turnover and protect against progression of diabetic glomerulosclerosis.
3 onse to hyperglycemia in the pathogenesis of diabetic glomerulosclerosis.
4 acellular matrix deposition is a hallmark of diabetic glomerulosclerosis.
5 be a major contributor to the development of diabetic glomerulosclerosis.
6 ations for the pathogenesis and treatment of diabetic glomerulosclerosis.
7 e that may play a role in the development of diabetic glomerulosclerosis.
8 glomerulosclerosis, and proteinuria seen in diabetic glomerulosclerosis.
9 renal parenchymal disease other than classic diabetic glomerulosclerosis.
10 ntion with GS-444217 significantly inhibited diabetic glomerulosclerosis and reduced renal dysfunctio
11 y, dialysis at presentation, the presence of diabetic glomerulosclerosis, and greater tubular atrophy
12 om biopsies performed from 1995 to 2011 with diabetic glomerulosclerosis as the only glomerular disea
13 ot PENT, was correlated with the severity of diabetic glomerulosclerosis, as assessed pathologically.
14 er CTGF is implicated in the pathogenesis of diabetic glomerulosclerosis, cultured rat mesangial cell
15 ar pericyte that secretes excess collagen in diabetic glomerulosclerosis), ET-1 increased mRNA and pr
18 lic mechanical strain, all causal factors in diabetic glomerulosclerosis, markedly induced the expres
20 e extracellular matrix (ECM) accumulation in diabetic glomerulosclerosis may be partly due to decreas
23 ether ILK is involved in the pathogenesis of diabetic glomerulosclerosis, we have analyzed the distri
24 s of hypertensive arterionephrosclerosis and diabetic glomerulosclerosis were frequent but typically
25 h type 2 DM may not always be due to classic diabetic glomerulosclerosis, which is associated with al
26 ndividuals with type 2 DM and CRI not due to diabetic glomerulosclerosis will receive appropriate int