Epithelial–mesenchymal plasticity in kidney fibrosis
Issued Date
2023-01-01
Resource Type
ISSN
1526954X
eISSN
1526968X
Scopus ID
2-s2.0-85162702757
Journal Title
Genesis (United States)
Rights Holder(s)
SCOPUS
Bibliographic Citation
Genesis (United States) (2023)
Suggested Citation
Hadpech S., Thongboonkerd V. Epithelial–mesenchymal plasticity in kidney fibrosis. Genesis (United States) (2023). doi:10.1002/dvg.23529 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/87757
Title
Epithelial–mesenchymal plasticity in kidney fibrosis
Author(s)
Author's Affiliation
Other Contributor(s)
Abstract
Epithelial–mesenchymal transition (EMT) is an important biological process contributing to kidney fibrosis and chronic kidney disease. This process is characterized by decreased epithelial phenotypes/markers and increased mesenchymal phenotypes/markers. Tubular epithelial cells (TECs) are commonly susceptible to EMT by various stimuli, for example, transforming growth factor-β (TGF-β), cellular communication network factor 2, angiotensin-II, fibroblast growth factor-2, oncostatin M, matrix metalloproteinase-2, tissue plasminogen activator (t-PA), plasmin, interleukin-1β, and reactive oxygen species. Similarly, glomerular podocytes can undergo EMT via these stimuli and by high glucose condition in diabetic kidney disease. EMT of TECs and podocytes leads to tubulointerstitial fibrosis and glomerulosclerosis, respectively. Signaling pathways involved in EMT-mediated kidney fibrosis are diverse and complex. TGF-β1/Smad and Wnt/β-catenin pathways are the major venues triggering EMT in TECs and podocytes. These two pathways thus serve as the major therapeutic targets against EMT-mediated kidney fibrosis. To date, a number of EMT inhibitors have been identified and characterized. As expected, the majority of these EMT inhibitors affect TGF-β1/Smad and Wnt/β-catenin pathways. In addition to kidney fibrosis, these EMT-targeted antifibrotic inhibitors are expected to be effective for treatment against fibrosis in other organs/tissues.