Cellular and molecular mechanisms in kidney fibrosis

被引：557

作者：

Duffield, Jeremy S. ^{[1
,2
,3
]}

机构：

[1] Univ Washington, Div Nephrol, Dept Pathol & Med, Inst Stem Cell & Regenerat Med, Seattle, WA 98195 USA

[2] Univ Washington, Kidney Res Inst, Seattle, WA 98195 USA

[3] Biogen Idec Inc, Cambridge, MA 02142 USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2014年 / 124卷 / 06期

关键词：

MEMBRANE-TYPE-1; MATRIX-METALLOPROTEINASE; PERICYTE-MYOFIBROBLAST TRANSITION; EPITHELIAL-CELLS; MESENCHYMAL TRANSITION; RENAL FIBROSIS; MAJOR SOURCE; COLLAGEN; RECEPTOR; MACROPHAGES; FIBROBLASTS;

D O I：

10.1172/JCI72267

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Fibrosis is a characteristic feature of all forms of chronic kidney disease. Deposition of pathological matrix in the interstitial space and within the walls of glomerular capillaries as well as the cellular processes resulting in this deposition are increasingly recognized as important factors amplifying kidney injury and accelerating nephron demise. Recent insights into the cellular and molecular mechanisms of fibrogenesis herald the promise of new therapies to slow kidney disease progression. This review focuses on new findings that enhance understanding of cellular and molecular mechanisms of fibrosis, the characteristics of myofibroblasts, their progenitors, and molecular pathways regulating both fibrogenesis and its resolution.

引用

页码：2299 / 2306

页数：8

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