ArticleRenal failure2026
Curcumin regulates ferroptosis by activating α7 nicotinic acetylcholine receptor to improve sepsis-induced acute kidney injury.
Article in Renal failure, 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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a frequent complication of sepsis. It has been reported that curcumin can alleviate sepsis-associated AKI (SA-AKI). This study aims to elucidate the regulatory effects and mechanisms of curcumin on ferroptosis in the context of SA-AKI. In this study, septic mice and lipopolysaccharide-stimulated HK-2 cells were employed to simulate the pathological conditions of SA-AKI. The status of renal injury and ferroptosis-related indicators was determined to assess the regulatory effect of curcumin on ferroptosis in SA-AKI. Furthermore, the expression of α7 nicotinic acetylcholine receptor (α7nAChR) was intervened to investigate the specific protective mechanism of curcumin in SA-AKI. Finally, the nuclear factor erythroid 2-related factor 2 (NRF2) inhibitor ML385 was incorporated to further elucidate the potential pathway through which α7nAChR regulates ferroptosis. The results demonstrated that curcumin exerted a significant protective effect on SA-AKI cells and animal models, markedly reducing cellular damage and renal injury in mice, attenuating the inflammatory response, and effectively inhibiting ferroptosis in renal cells and tissues. Furthermore, curcumin treatment upregulated the expression of α7nAChR in both SA-AKI cells and animal models. Nevertheless, the inhibition of α7nAChR expression partially counteracted the ameliorative effects of curcumin on injury and ferroptosis in SA-AKI cells and animal models. The overexpression of α7nAChR attenuated LPS-induced ferroptosis in HK-2 cells, whereas ML385 reversed the inhibitory impact of α7nAChR upregulation on cellular ferroptosis. In conclusion, these findings indicate that curcumin suppresses ferroptosis by upregulating α7nAChR to activate the antioxidant capacity of NRF2, thereby providing a protective effect against SA-AKI.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.