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Updated: Aug 21, 2026

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells
Published on: June 20, 2018
[Signal transduction on transdifferentiation of renal tubular epithelial cell]
1Renal Division, Department of Medicine, First Hospital and Institute of Nephrology, Peking University, Beijing 100034.
Abstract:
It is an important cell biological phenomenon that epithelial cells transit into mesenchymal cells under special physiological and pathological condition. In recent years, it has been known that epithelial-mesenchymal-transition may be mediated by several intracellular signaling pathways, such as MAPK, Rho, Src, PI3 kinase and Smads. Renal tubular epithelial cells have been observed to transit to myo-fibroblasts in renal diseases. However, the intracellular signaling pathways are rarely known. The progress on this field is reviewed.
Insights
Epithelial cells can transform into mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT). This review explores the signaling pathways involved in EMT, particularly in kidney diseases.
Area of Science:
- Cell Biology
- Molecular Biology
- Pathophysiology
Context:
- Epithelial-mesenchymal transition (EMT) is a critical cellular process observed in development and disease.
- EMT involves the transformation of stationary epithelial cells into migratory mesenchymal cells.
- Signaling pathways like MAPK, Rho, Src, PI3 kinase, and Smads are implicated in mediating EMT.
Purpose:
- To review the current understanding of intracellular signaling pathways regulating epithelial-mesenchymal transition (EMT).
- To highlight the specific role of EMT in renal diseases, focusing on renal tubular epithelial cells transitioning to myo-fibroblasts.
- To identify gaps in knowledge regarding the signaling mechanisms underlying EMT in kidney pathologies.
Summary:
- This review synthesizes information on the molecular mechanisms driving epithelial-mesenchymal transition (EMT).
- It details the involvement of key intracellular signaling cascades in this cellular reprogramming.
- The focus extends to the understudied signaling pathways governing EMT in the context of renal tubular cells and kidney disease progression.
Impact:
- Provides a comprehensive overview of EMT signaling pathways for researchers in cell biology and nephrology.
- Identifies critical knowledge gaps concerning EMT in renal pathology, guiding future research directions.
- Enhances understanding of cellular plasticity in kidney diseases, potentially informing therapeutic strategies.
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