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Rapamycin Is Not Protective against Ischemic and Cisplatin-Induced Kidney Injury
N V Andrianova1,2, L D Zorova2,3, V A Babenko2,3
1Lomonosov Moscow State University, Faculty of Bioengineering and Bioinformatics, Moscow, 119992, Russia.
Biochemistry. Biokhimiia
|December 25, 2019
Summary
Rapamycin, an autophagy activator, did not protect against acute kidney injury (AKI) in models of ischemia or cisplatin exposure. This suggests mTOR inhibition alone is insufficient for AKI treatment, necessitating further research into complex protective mechanisms.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- Autophagy is crucial in acute kidney injury (AKI) pathogenesis.
- Autophagy activators show promise, but rapamycin's effect on AKI is unclear.
Purpose of the Study:
- To investigate rapamycin's impact on ischemic and cisplatin-induced AKI models.
- To determine if rapamycin ameliorates kidney damage and enhances autophagy.
Main Methods:
- In vivo studies using ischemia/reperfusion and cisplatin models.
- In vitro studies on renal tubular cells (RTCs) with oxygen-glucose deprivation or cisplatin.
- Assessed kidney function via blood urea nitrogen, serum creatinine, and neutrophil gelatinase-associated lipocalin.
- Measured cell viability and proliferation using MTT assay and RTCA iCELLigence system.
Main Results:
- Rapamycin inhibited mTOR signaling but did not enhance autophagy or protect against AKI.
- In vitro, rapamycin showed anti-proliferative effects on RTCs but no protection against injury.
- Rapamycin failed to improve kidney function markers in AKI models.
Conclusions:
- Rapamycin does not prevent AKI from ischemia or cisplatin, challenging its role as an autophagy-mimetic nephroprotective agent.
- Caloric restriction's protective effects may involve broader mechanisms beyond mTOR inhibition.
- Further studies are needed to clarify rapamycin's role and potential adverse effects in AKI treatment.
