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Updated: Aug 11, 2026
Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions
Published on: June 13, 2025
Modulation of renal tubular cell survival: where is the evidence?
C Lorz1, A Benito-Martin, P Justo
1Renal and Vascular Research Laboratory, Division of Nephrology, Fundacion Jimenez Diaz, Universidad Autonoma de Madrid and Fundacion Renal Iñigo Alvarez de Todelo, Madrid, Spain.
Abstract:
Tubular cell loss is prominent both in acute and chronic renal failure. Apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The potential role of apoptosis ranges from induction and progression to repair of renal injury. However, therapeutic interest has focused in preventing the apoptotic loss of tubular cells that leads to acute and chronic renal failure. Death ligands and receptors, such as tumor necrosis factor and Fas ligand, proapoptotic and antiapoptotic Bcl2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal cell injury. Nevertheless, the precise role of these proteins is unclear, and the participation of most known apoptosis regulatory proteins has not been studied. We now review the role of apoptosis in renal injury, the potential molecular targets of therapeutic intervention, the therapeutic weapons to modulate the activity of these targets and the few examples of therapeutic intervention on apoptosis, with emphasis in acute renal failure.
Insights
Apoptosis, programmed cell death, significantly contributes to tubular cell loss in acute and chronic kidney failure. Therapeutic strategies aim to prevent this cell loss by targeting apoptosis regulatory mechanisms in renal injury.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Medicine
Background:
- Tubular cell loss is a key feature of acute and chronic kidney failure.
- Apoptosis plays a critical role in regulating kidney cell numbers during injury and repair.
- Existing research highlights the involvement of apoptosis in renal injury, but precise mechanisms remain unclear.
Purpose of the Study:
- To review the role of apoptosis in renal injury.
- To identify potential molecular targets for therapeutic intervention.
- To discuss therapeutic strategies for modulating apoptosis in kidney disease, particularly acute renal failure.
Main Methods:
- Literature review of studies on apoptosis in renal injury.
- Analysis of regulatory mechanisms including death ligands, Bcl2 family, and caspases.
- Examination of therapeutic interventions targeting apoptosis in preclinical models.
Main Results:
- Apoptosis is implicated in the progression and severity of renal injury.
- Specific proteins like death receptors, Bcl2 family members, and caspases are involved in renal apoptosis.
- Therapeutic interventions targeting apoptosis pathways show promise in preclinical studies for acute renal failure.
Conclusions:
- Apoptosis is a critical factor in tubular cell loss during renal failure.
- Targeting apoptosis pathways represents a promising therapeutic avenue for kidney diseases.
- Further research is needed to elucidate the precise roles of apoptosis regulators and optimize therapeutic strategies.
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