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Updated: Jun 3, 2025
09:40
Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells
Published on: June 20, 2018
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Proteinuria and tubular cells: Plasticity and toxicity
Anna Faivre1,2, Thomas Verissimo1, Sophie de Seigneux1,2
1Department of Medicine, Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland.
Acta Physiologica (Oxford, England)
|January 11, 2025
Summary
Proteinuria, a key factor in chronic kidney disease (CKD) progression, damages kidney tubular epithelial cells. Understanding these effects reveals new therapeutic targets for CKD.
Area of Science:
- Nephrology
- Cell Biology
- Biochemistry
Background:
- Proteinuria is a primary indicator of chronic kidney disease (CKD) progression.
- While glomerular damage initiates proteinuria, tubular epithelial cells are significantly impacted, driving disease advancement.
- Interventions reducing proteinuria are currently the most effective nephroprotective strategies.
Purpose of the Study:
- To elucidate mechanisms of tubular protein handling.
- To explore the detrimental effects of proteinuria on tubular epithelial cell function.
- To review the dynamic phenotypic changes in nephrons due to proteinuria.
Main Methods:
- This study is a narrative review.
- Literature search conducted on PubMed from inception to 2024.
- Focus on the impact of proteinuria on tubular cells.
Main Results:
- Proteinuria induces toxic effects on tubular epithelial cells via signaling pathways, ER stress, oxidative stress, and metabolic changes.
- Plasma proteins trigger detrimental cellular responses.
- The review details phenotypic alterations in nephrons caused by proteinuria.
Conclusions:
- The interaction between proteinuria and tubular cells is critical for CKD progression.
- Identifying these mechanisms offers potential therapeutic targets for kidney disease.
- This review provides insights into novel therapeutic strategies for managing CKD.
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