Renal fibrosis: not just PAI-1 in the sky.
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.
Fogo
Agnes B
AB
Department of Pathology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA. agnes.fogo@vanderbilt.edu
D000818:Animals; D002465:Cell Movement; D005109:Extracellular Matrix / Q000502:physiology; D005355:Fibrosis; D006801:Humans; D007668:Kidney / Q000473:pathology* / Q000503:physiopathology; D007674:Kidney Diseases / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D008264:Macrophages / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D009154:Mutation; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics / Q000502:physiology*; D051381:Rats
D017395:Plasminogen Activator Inhibitor 1