Key result
Mdivi-1 attenuates doxorubicin-induced renal dysfunction and mitochondrial damage in aged rats.
Why the study?
The role of excessive mitochondrial fission in doxorubicin-induced nephrotoxicity, particularly in the context of renal aging, remains unclear.
Does Mdivi-1 reduce doxorubicin-induced nephrotoxicity in a rat model of accelerated renal aging?
Does Mdivi-1 reduce doxorubicin-induced nephrotoxicity in a rat model of accelerated renal aging?
Inhibition of mitochondrial fission with Mdivi-1 mitigates doxorubicin-induced nephrotoxicity in a rat model of accelerated renal aging, suggesting a potential therapeutic strategy to protect kidneys during chemotherapy.
Answers are grounded in this paper and cite their sources.
Should not yet change practice in elderly chemotherapy patients; leaves open translation of Mdivi-1 renoprotection from aged rat models.
The clinical use of doxorubicin (DOX), an effective chemotherapeutic drug for breast cancer, is limited by off-target nephrotoxicity, which is exacerbated in elderly patients. While excessive mitochondrial fission is known to contribute to DOX-induced cardiotoxicity, its role in DOX-induced nephrotoxicity, particularly in the context of renal aging, remains unclear. To explore this and investigate the therapeutic potential of the mitochondrial fission inhibitor Mdivi-1, female Wistar rats with D-galactose-induced accelerated renal aging were allocated into four groups: vehicle, DOX, DOX+Mdivi-1 co-treatment, and DOX+Mdivi-1 post-treatment. DOX administration resulted in significant renal dysfunction, oxidative stress, inflammation, and histopathological damage. Mitochondrial dysfunction along with the increased expression of fission protein, decreased fusion proteins, and activation of apoptotic markers and PINK1 expression were also evident. Remarkably, both co-treatment and post-treatment with Mdivi-1 comparably and significantly attenuated DOX-induced renal damage. This study suggests that Mdivi-1 mitigates DOX-induced nephrotoxicity in the aged kidney by modulating mitochondrial dynamics, suppressing oxidative stress and inflammation, and inhibiting apoptosis. These findings highlight mitochondrial fission as a promising therapeutic target for the treatment of doxorubicin toxicity and provide further support for the possible use of Mdivi-1 as a therapeutic strategy to protect the kidneys of elderly breast cancer patients undergoing chemotherapy.
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Kobroob et al. (2026) studied Doxorubicin-induced nephrotoxicity in accelerated renal aging (n=44). Mdivi-1 vs. Doxorubicin alone was evaluated on Renal function (BUN, serum creatinine, KIM-1), oxidative stress, and mitochondrial function (p=<0.05). Mdivi-1 administered as either a co-treatment or post-treatment significantly attenuated doxorubicin-induced renal dysfunction, oxidative stress, and mitochondrial damage in aged rats.
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