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• W2024441465 abstract "A delicate balance exists between ECM synthesis and degradation such that interruption of the corresponding pathways results in increased plasminogen activator inhibitor-1 (PAI-1), pathological matrix accumulation, and glomerulosclerosis. A new study demonstrates that therapy with a mutant PAI-1 increases matrix turnover and reduces glomerulosclerosis by competing with endogenous PAI-1, suggesting therapeutic utility in the treatment of fibrotic renal disease." @default.
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• W2024441465 date "2003-08-01" @default.
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• W2024441465 title "Renal fibrosis: not just PAI-1 in the sky" @default.
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• W2024441465 doi "https://doi.org/10.1172/jci19375" @default.
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