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Podocyte dysfunction in kidney diseases: Mechanisms and therapeutic advances
Shams Ismayilova1, Onur Mutlu2, Jamila Bayramova3
1Department of Stem Cell Sciences, Institute of Health Sciences, Ege University, İzmir, Türkiye.
Science Progress
|August 10, 2026
Summary
Podocyte damage drives proteinuric kidney diseases. This review explores podocyte biology, injury pathways, and emerging therapies, emphasizing podocyte-focused treatments for preserving kidney function.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Medicine
Background:
- Podocytes are crucial visceral epithelial cells forming the glomerular filtration barrier.
- Podocyte injury, including foot process effacement and apoptosis, underlies proteinuric glomerular diseases.
- These diseases include minimal change disease, FSGS, membranous nephropathy, and diabetic nephropathy.
Purpose of the Study:
- To review podocyte biology and its role in kidney function.
- To examine molecular pathways implicated in podocyte damage.
- To discuss current and future therapeutic strategies for podocytopathies.
Main Methods:
- This is a narrative review synthesizing existing literature.
- Key molecular pathways (RhoA/ROCK, TGF-β, mTOR, oxidative stress) were analyzed.
- Clinical presentations and treatment options were examined.
Main Results:
- Podocyte damage is central to the pathogenesis of major proteinuric glomerular diseases.
- Multiple molecular pathways contribute to podocyte injury.
- A range of treatments, from RAAS blockade to regenerative medicine, are being explored.
Conclusions:
- Podocyte-focused therapies are essential for managing glomerular diseases.
- Preserving podocyte integrity is key to preventing progressive kidney disease.
- Personalized molecular therapies and multidisciplinary research are vital for future advancements.
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