ArticleJournal of toxicology2026
Empagliflozin Alleviates Arsenic Trioxide-Induced Nephrotoxicity by Activating the SIRT1/Akt/Nrf2 Pathway.
Article in Journal of toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Empagliflozin Alleviates Arsenic Trioxide-Induced Nephrotoxicity by Activating the SIRT1/Akt/Nrf2 Pathway.Journal of toxicology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arsenic trioxide (ATO), utilized in the treatment of acute promyelocytic leukemia (APL), presents significant renal toxicity that restricts its clinical usage. The potential effects of empagliflozin (EMPA) on ATO-induced nephrotoxicity remain unexplored. This study aims to investigate whether EMPA can alleviate ATO-induced nephrotoxicity in both animal and cellular models, as well as to further explore the underlying mechanisms. EMPA can improve renal function in mice and alleviate ATO-induced structural damage to the kidneys. EMPA treatment effectively inhibits ATO-induced oxidative stress and reduces apoptosis. EMPA significantly decreases the production of ROS in cultured HEK293T cells, lowers the apoptotic rate, and safeguards mitochondrial function. EMPA upregulates the SIRT1/Akt/Nrf2 pathway and addresses ATO-induced autophagy dysfunction. These findings suggest that EMPA may ameliorate ATO-induced renal toxicity by activating the SIRT1/Akt/Nrf2 signaling pathway, which is associated with the suppression of oxidative stress, reduction of apoptosis, and protection of mitochondrial functionality.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.