Evidence map›Paper›PMID 42543258›Full record

ArticleDiabetes, obesity & metabolism2026

Sodium Butyrate Attenuates Renal Fibrosis by Regulating Glycolysis and Histone H4K12 Lactylation in Diabetic Kidney Disease.

Ping He, Mingxiu Wang, Hang Mei, Yue Liu, Min Wang, He Sun, Yali Peng, Xuan Ban, Yue Wang, Xiaofang Tang and 1 more

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In one paragraph

Article in Diabetes, obesity & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
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1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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.

2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Ping HeDepartment of Nephrology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Mingxiu WangDepartment of Nephrology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-4906-0795
Hang MeiDepartment of Nephrology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yue LiuDepartment of Nephrology, The Second Hospital of Jilin University, Changchun, Jilin Province, China.ORCID 0009-0003-2641-3102
Min WangDepartment of Nephrology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, China.
He SunDepartment of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
Yali PengDepartment of Nephrology, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
Xuan BanDepartment of Nephrology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yue WangDepartment of Nephrology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaofang TangPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qiuling FanDepartment of Nephrology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Funding

Anhui Provincial Department of Education University Scientific Research Projects 2025AHGXZK40765National Natural Science Foundation of China 82070754National Natural Science Foundation of China 82400529National Natural Science Foundation of China 82500875Shanghai Pujiang Program 22PJD061Shanghai Pujiang Program 23PJ1410700
6 · The paper itself

Abstract

backgroundThe role of histone lactylation in diabetes associated renal fibrosis remains poorly defined. In this study, we investigated the contribution of histone H4 lysine 12 lactylation (H4K12la) to abnormal glycolysis and renal fibrogenesis in diabetic kidney disease (DKD) and evaluated sodium butyrate (NaB) as a potential therapeutic modulator.

methodsIn this study, db/db mice (Bks. Cg-

resultsWe found that H4K12la expression was significantly increased in diabetic kidneys, which was closely associated with enhanced glycolysis related fibrosis. Analysis of kidney biopsy tissues from patients with DKD confirmed that H4K12la levels were significantly elevated. CUT&Tag sequencing in HK-2 cells revealed enrichment of H4K12la at genes involved in metabolic pathways, including the promoter region of HIF1A. In vivo and in vitro experiments demonstrated that NaB treatment suppressed the expression of glycolytic enzymes hexokinase 2 (HK2) and lactate dehydrogenase A (LDHA), reduced lactate production, improved renal function, and attenuated kidney fibrosis under diabetic conditions. Mechanistically, these effects were associated with decreased H4K12la enrichment at the HIF1A promoter.

conclusionsCollectively, our findings identify aberrant renal glycolysis and H4K12la as key drivers of diabetic renal fibrosis and suggest that NaB mitigates fibrosis by modulating glycolysis-dependent H4K12la and HIF-1α signalling.

Indexed as

Butyric AcidDiabetic NephropathiesGlycolysisHistonesKidneyAnimalsCell LineFibrosisHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMiceButyric AcidHistonesHypoxia-Inducible Factor 1, alpha Subunitdiabetic kidney diseaseglycolysishistone H4 lysine 12 lactylationhypoxia‐inducible factor‐1αsodium butyrate

Identifiers

PMID42543258
PMCPMC13538752

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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.