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Published on: March 4, 2022
EMT and proteinuria as progression factors
1Department of Nephrology and Rheumatology, Georg-August-University Medical Center, Göttingen, Germany. fstrutz@gwdg.de
Tubulointerstitial fibrosis, a key feature of chronic kidney disease, involves myofibroblast activation and extracellular matrix buildup. Proteinuria and epithelial-mesenchymal transition (EMT) contribute to fibrosis, but their precise relationship requires further study.
Area of Science:
- Nephrology
- Renal Pathology
- Cell Biology
Background:
- Tubulointerstitial fibrosis is a hallmark of chronic kidney disease, characterized by extracellular matrix accumulation.
- Myofibroblasts, derived from various cell types, are the primary mediators of matrix deposition.
- Inflammation and proteinuria are implicated in the progression of renal fibrosis.
Purpose of the Study:
- To explore the mechanisms driving tubulointerstitial fibrosis in chronic kidney disease.
- To investigate the roles of proteinuria and epithelial-mesenchymal transition (EMT) in renal fibrosis.
- To clarify the relationship between proteinuria and EMT in the context of kidney disease progression.
Main Methods:
- Review of existing literature on tubulointerstitial fibrosis, myofibroblast activation, and renal disease.
- Analysis of cellular sources of myofibroblasts, including fibroblasts, epithelial cells, and stem cells.
- Examination of the signaling pathways involved in epithelial-mesenchymal transition (EMT).
Main Results:
- Myofibroblast activation and extracellular matrix accumulation are central to tubulointerstitial fibrosis.
- Proteinuria can directly injure tubular cells and promote inflammation, contributing to fibrosis.
- Epithelial-mesenchymal transition (EMT) is a key process where epithelial cells transform into matrix-producing myofibroblasts.
- Both proteinuria severity and EMT extent correlate with declining renal function.
Conclusions:
- Tubulointerstitial fibrosis is a complex process involving myofibroblasts, inflammation, and matrix deposition.
- Proteinuria and EMT are significant contributors to chronic kidney disease progression.
- While therapeutic strategies targeting proteinuria and EMT show promise, their interconnectedness needs further investigation.
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