期刊
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
卷 19, 期 2, 页码 329-338出版社
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2007040510
关键词
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资金
- NIDDK NIH HHS [R01 DK060508, DK 60508] Funding Source: Medline
Plasminogen activator inhibitor-1 (PAI-1) has been implicated in renal fibrosis. In vitro, PAI-1 inhibits plasmin generation, and this decreases mesangial extracellular matrix turnover. PAI-1R, a mutant PAI-1, increases glomerular plasmin generation, reverses PAI-1 inhibition of matrix degradation, and reduces disease in experimental glomerulonephritis. This study sought to determine whether short-term administration of PAI-1 R could slow the progression of glomerulosclerosis in the db/db mouse, a model of type 2 diabetes in which mesangial matrix accumulation is evident by 20 wk of age. Untreated uninephrectomized db/db mice developed progressive albuminuria and mesangial matrix expansion between weeks 20 and 22, associated with increased renal mRNA encoding alpha 1(I) and (IV) collagens and fibronectin. Treatment with PAI-1 R prevented these changes without affecting body weight, blood glucose, glycosylated hemoglobin, creatinine, or creatinine clearance; therefore, PAI-1 R may prevent progression of glomerulosclerosis in type 2 diabetes.
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