Mechanistic connection between inflammation and fibrosis

被引:241
作者
Lee, Soo Bong
Kalluri, Raghu [1 ,2 ,3 ]
机构
[1] Beth Israel Deaconess Med Ctr, Dept Med, Div Matrix Biol, CLS 11086, Boston, MA 02215 USA
[2] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02215 USA
[3] Harvard Massachusetts Inst Technol, Div Hlth Sci & Technol, Boston, MA USA
基金
美国国家卫生研究院;
关键词
B cell; fibrosis; inflammation; leukocyte; macrophage; T cell; FACTOR-KAPPA-B; UNILATERAL URETERAL OBSTRUCTION; MONONUCLEAR-CELL SUBSETS; TYPE-1; DIABETIC-PATIENTS; RENAL FIBROSIS; MONOCLONAL-ANTIBODIES; MAST-CELLS; CRESCENTIC GLOMERULONEPHRITIS; PODOCYTE DEPLETION; GLOMERULAR INJURY;
D O I
10.1038/ki.2010.418
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Fibrosis of the kidney is caused by the prolonged injury and deregulation of normal wound healing and repair processes, and by an excess deposition of extracellular matrices. Despite intensive research, our current understanding of the precise mechanism of fibrosis is limited. There is a connection between fibrotic events involving inflammatory and noninflammatory glomerulonephritis, inflammatory cell infiltration, and podocyte loss. The current review will discuss the inflammatory response after renal injury that leads to fibrosis in relation to non-inflammatory mechanisms.
引用
收藏
页码:S22 / S26
页数:5
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