Abstract
Epithelial-mesenchymal transition (EMT) is described as the process in which injured renal tubular epithelial cells undergo a phenotype change, acquiring mesenchymal characteristics and morphing into fibroblasts. Initially, it was widely thought of as a critical mechanism of fibrogenesis underlying chronic kidney disease. However, evidence that renal tubular epithelial cells can cross the basement membrane and become fibroblasts in the renal interstitium is rare, leading to debate about the existence of EMT. Recent research has demonstrated that after injury, renal tubular epithelial cells acquire mesenchymal characteristics and the ability to produce a variety of profibrotic factors and cytokines, but remain attached to the basement membrane. On this basis, a new concept of “partial epithelial-mesenchymal transition (pEMT)” was proposed to explain the contribution of renal epithelial cells to renal fibrogenesis. In this review, we discuss the concept of pEMT and the most recent findings related to this process, including cell cycle arrest, metabolic alternation of epithelial cells, infiltration of immune cells, epigenetic regulation as well as the novel signaling pathways that mediate this disturbed epithelial-mesenchymal communication. A deeper understanding of the role and the mechanism of pEMT may help in developing novel therapies to prevent and halt fibrosis in kidney disease.
Highlights
The progress of renal fibrosis – glomerulosclerosis and tubulointerstitial fibrosis – is characterized by an excessive deposition of extracellular matrix (ECM) components in the tubular interstitium
Given that TGF-β1 is a potent inducer of partial Epithelial-mesenchymal transition (EMT) and all three fibrotic injuries cited by Liu et al (2020) can induce EMT, these results suggest that tubule-derived exosomes play an essential role in driving renal fibroblast activation and fibrogenesis
All cell types present in the kidney including epithelial cells, endothelial cells, mesangial cells, as well as immune cells contribute to the progression of chronic kidney diseases
Summary
The progress of renal fibrosis – glomerulosclerosis and tubulointerstitial fibrosis – is characterized by an excessive deposition of extracellular matrix (ECM) components in the tubular interstitium. Grande et al (2015) demonstrated that Snail1 induced partial EMT of renal tubular cells, which produces fibrogenic cytokines to promote myofibroblasts proliferation and macrophage recruitment.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
