ArticleRenal failure2025
Roxadustat alleviates cisplatin-induced acute kidney injury by regulating fatty acid oxidation and mitochondrial function.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Roxadustat attenuates contrast-induced acute kidney injury potentially mediated via the Nrf2/HO-1 signaling pathway.Renal failure · 2026Article
- Daphnetin alleviates cisplatin-induced acute kidney injury by inhibiting the HIF-1α signaling pathway.In vitro cellular & developmental biology. Animal · 2026Article
- ACSL5 programs fatty acid metabolism and mitochondrial fitness to sustain pathogenic T cells and exacerbate Sjögren's syndrome.International journal of biological sciences · 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
aimsThis study aimed to elucidate the role and function of roxadustat, a small molecule hypoxia-inducible factor (HIF) stabilizer, on cisplatin-induced acute kidney injury (AKI)
methodsWe investigated the effects of roxadustat (10 mg/kg) in a cisplatin-induced AKI model in mice. After a 48-hour pretreatment with the intraperitoneal injection of roxadustat, cisplatin was administered at a dose of 20 mg/kg by intraperitoneal injection. We also examined the role of roxadustat (10 μM) on HK-2 cells stimulated by cisplatin (20 μg/mL).
resultsPretreatment with roxadustat significantly improved kidney function in the AKI model, as evidenced by reductions of Scr and BUN, and alleviated cisplatin-induced kidney morphology lesions. Roxadustat also remarkably decreased the expression of KIM-1 and NGAL. Furthermore, roxadustat significantly abolished the expression of Bax and cleaved caspase 3, two apoptosis marker proteins. Mechanistically, our study demonstrated that roxadustat could alleviate the deficiency of fatty acid oxidation (FAO) induced by cisplatin, as evidenced by the improvement of lipid accumulation and metabolic disorders in the roxadustat-treated group. Moreover, roxadustat effectively blocked mitochondrial damage, as evidenced by reduced mitochondrial swelling and fragmentation in the roxadustat-treated group. Simultaneously, roxadustat also partially rescued the expression of mitochondrial fusion proteins, including OPA1, MFN1, and MFN2.
conclusionWe demonstrated that roxadustat exerts a protective role in cisplatin-treated mice and HK-2 cells, which might be due to amelioration of FAO deficiency and suppression of mitochondrial damage.
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.