Epithelial-mesenchymal transition in tissue repair and degeneration

被引:20
|
作者
Youssef, Khalil Kass [1 ]
Nieto, M. Angela [1 ,2 ]
机构
[1] Inst Neurociencias CSIC UMH, Sant Joan dAlacant, Spain
[2] ISCIII, Ctr Invest Biomed Red Enfermedades Raras, CIBERER, Madrid, Spain
关键词
NF-KAPPA-B; TRANSCRIPTION FACTOR SNAIL; E-CADHERIN EXPRESSION; ACUTE KIDNEY INJURY; CELL-CYCLE ARREST; TUMOR-METASTASIS; RENAL FIBROSIS; CANCER-CELLS; MULLER GLIA; TGF-BETA;
D O I
10.1038/s41580-024-00733-z
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Epithelial-mesenchymal transitions (EMTs) are the epitome of cell plasticity in embryonic development and cancer; during EMT, epithelial cells undergo dramatic phenotypic changes and become able to migrate to form different tissues or give rise to metastases, respectively. The importance of EMTs in other contexts, such as tissue repair and fibrosis in the adult, has become increasingly recognized and studied. In this Review, we discuss the function of EMT in the adult after tissue damage and compare features of embryonic and adult EMT. Whereas sustained EMT leads to adult tissue degeneration, fibrosis and organ failure, its transient activation, which confers phenotypic and functional plasticity on somatic cells, promotes tissue repair after damage. Understanding the mechanisms and temporal regulation of different EMTs provides insight into how some tissues heal and has the potential to open new therapeutic avenues to promote repair or regeneration of tissue damage that is currently irreversible. We also discuss therapeutic strategies that modulate EMT that hold clinical promise in ameliorating fibrosis, and how precise EMT activation could be harnessed to enhance tissue repair. During embryonic epithelial-mesenchymal transition, epithelial cells undergo substantial phenotypic changes and acquire migration capacity. This Review compares embryonic and adult non-cancer EMTs and discusses the role of EMTs in adult tissue repair and fibrosis, highlighting therapeutic opportunities to modulate EMT to reduce fibrosis and promote repair.
引用
收藏
页码:720 / 739
页数:20
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