Modulation of glomerulosclerosis

被引:26
作者
Ma, Li-Jun [1 ]
Fogo, Agnes B. [1 ]
机构
[1] Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA
关键词
angiotensin; PAI-1; TGF-beta; regression; thymosin beta-4;
D O I
10.1007/s00281-007-0087-y
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
Regardless of the initial injury, the long-term consequence for the patient depends upon the ensuing balance of profibrotic vs reparative modulators activated. The glomerulus has some capacity for repair. Even when sclerosis has developed with accumulation of extracellular matrix, this lesion may be remodeled, with a change in balance between profibrotic and antifibrotic and collagen synthesis vs proteolytic mediators. We will focus here on the interplay between mediators of fibrosis and reparative mechanisms and potential regression of fibrosis. Based on the clinical efficacy of interventions that inhibit angiotensin, we will focus on factors related to the renin-angiotensin system.
引用
收藏
页码:385 / 395
页数:11
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