Related Experiment Video
Updated: Aug 20, 2025
10:31
Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
270
Cellular phenotypic transitions in diabetic nephropathy: An update
Yiling Cao1, Ji-Hong Lin2, Hans-Peter Hammes2
1Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Frontiers in Pharmacology
|November 21, 2022
Summary
Diabetic nephropathy (DN) causes kidney fibrosis through cellular phenotypic switching. Understanding these transitions and molecular pathways is key to developing targeted therapies for this diabetes complication.
Area of Science:
- Nephrology
- Diabetology
- Cellular Biology
Background:
- Diabetic nephropathy (DN) is a leading cause of end-stage renal disease (ESRD).
- Renal fibrosis is the critical pathological outcome in DN.
- Cellular phenotypic switching is implicated in the development of renal fibrosis in DN.
Purpose of the Study:
- To discuss the pathophysiologic changes in DN.
- To delineate the origins of myofibroblasts and podocytes via phenotypic transitions.
- To highlight molecular signaling pathways involved in these transitions for therapeutic development.
Main Methods:
- Review of pathophysiologic changes in DN.
- Discussion of cellular origins contributing to fibrosis.
- Identification of key molecular signaling pathways.
Main Results:
- Cellular phenotypic switching contributes to renal fibrosis in DN.
- Various kidney cells reprogram into mesenchymal or podocyte-like cells.
- Specific molecular pathways drive these phenotypic transitions.
Conclusions:
- Phenotypic switching is a central mechanism in DN-associated renal fibrosis.
- Understanding these transitions offers insights into potential therapeutic targets.
- Targeted therapies for DN may be developed by modulating these pathways.
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