Fogo Agnes B
Department of Pathology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA.
J Clin Invest. 2003 Aug;112(3):326-8. doi: 10.1172/JCI19375.
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.
细胞外基质(ECM)的合成与降解之间存在着微妙的平衡,因此相应途径的中断会导致纤溶酶原激活物抑制剂-1(PAI-1)增加、病理性基质积聚和肾小球硬化。一项新研究表明,用突变型PAI-1进行治疗可通过与内源性PAI-1竞争来增加基质周转并减少肾小球硬化,这表明其在治疗纤维化肾病方面具有治疗价值。