Inflammation and EMT: an alliance towards organ fibrosis and cancer progression

被引:555
作者
Miguel Lopez-Novoa, Jose [2 ]
Angela Nieto, M. [1 ]
机构
[1] CSIC UMH, Inst Neurociencias, Alacant, Spain
[2] Univ Salamanca, Dept Fisiol & Farmacol, E-37008 Salamanca, Spain
关键词
inflammation; epithelial-mesenchymal transition; TGF-beta; TNF-alpha; NF-kappa B; NF-KAPPA-B; EPITHELIAL-MESENCHYMAL TRANSITION; UNILATERAL URETERAL OBSTRUCTION; TUMOR-CELL MIGRATION; TGF-BETA; ANGIOTENSIN-II; RENAL INJURY; E-CADHERIN; TUBULOINTERSTITIAL FIBROSIS; SNAIL TRANSCRIPTION;
D O I
10.1002/emmm.200900043
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
Recent advances in our understanding of the molecular pathways that govern the association of inflammation with organ fibrosis and cancer point to the epithelial to mesenchymal transition (EMT) as the common link in the progression of these devastating diseases. The EMT is a crucial process in the development of different tissues in the embryo and its reactivation in the adult may be regarded as a physiological attempt to control inflammatory responses and to 'heal' damaged tissue. However, in pathological contexts such as in tumours or during the development of organ fibrosis, this healing response adopts a sinister nature, steering these diseases towards metastasis and organ failure. Importantly, the chronic inflammatory microenvironment common to fibrotic and cancer cells emerges as a decisive factor in the induction of the pathological EMT.
引用
收藏
页码:303 / 314
页数:12
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