ArticleInflammation2026
β-Hydroxybutyrate Attenuates Diabetic Kidney Disease Partially Via β-hydroxybutyrylation of Nrf2.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Diabetic kidney disease (DKD) is one of the predominant microvascular complications in diabetes. In recent years, the nuclear factor E2-related factor 2 (Nrf2)-mediated anti-oxidative stress pathway is tightly regulated by multiple post-translational modifications, governing its role in countering oxidative stress and DKD pathogenesis. Recent studies have found that the principal constituent of ketone bodies, β-hydroxybutyrate (β-HB), not only serves as an alternative energy source, but also induced lysine β-hydroxybutyrylation (Kbhb), which has various unknown pathophysiological functions. Previous research reports that β-HB activates Nrf2 and then treats DKD, yet its underlying molecular mechanism remains unclear. To explore the mechanism of β-HB induced Kbhb in DKD, β-HB was administered in both in vivo and in vitro. Our results verified that exogenous β-HB supplementation alleviated dysglycolipidemia, inhibited proteinuria and renal dysfunction. Meanwhile, β-HB enhanced Nrf2 Kbhb modification, and activated the Nrf2 signaling to mitigate renal inflammatory-fibrotic injury in diabetes. However, inhibition of Kbhb partially reversed β-HB-mediated Nrf2 activation and nephroprotection. In conclusion, our data reveal that β-HB attenuates DKD, β-HB-induced Nrf2 Kbhb modification may be an important molecular mechanism in the pathogenesis and treatment of DKD.
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.