Evidence map›Paper›PMID 41203689›Full record

ArticleScientific reports2025

GADD45β inhibits hepatic lipogenesis through the AMPK/SREBP1 pathway via reducing the ubiquitination-mediated degradation of SIRT1.

Yuanyuan Xiao, Renjie Wang, Chaoyu Zhu, Qianqian Wang, Xinyi Wang, Wenjing Song, Shouxia Li, Fusong Jiang, Jun Yin, Li Wei

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. The Sirtuin Network: Linking NADDiabetes/metabolism research and reviews · 2026
    Review
  2. Review
4 · The record

Corrections and comments

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

10 authors.

Yuanyuan Xiao *Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Renjie Wang *School of Basic Medicine, Chongqing Medical University, Chongqing, People's Republic of China.
Chaoyu ZhuDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Qianqian WangDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Xinyi WangDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Wenjing SongDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Shouxia LiDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Fusong JiangDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Jun YinDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China. yinjun@sjtu.edu.cn.
Li WeiDepartment of Endocrinology and Metabolism, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China. 7250012162@shsmu.edu.cn.

Funding

Foundation of Shanghai University of Medicine and Health Sciences SSF-23-14-001Fundamental Research Funds for the Central Universities 24X010301321Institutional Project of Shanghai Sixth People's Hospital ynhglg202405Shanghai Municipal Science and Technology Commission Project 20ZR1442500
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a globally increasing metabolic disorder associated with serious health complications. The molecular mechanisms linking stress-response proteins to hepatic lipogenesis in MASLD remain poorly understood. Here, we identified GADD45β as a key suppressor of de novo lipogenesis through SIRT1 stabilization. In both methionine-choline-deficient (MCD) diet-fed mice and palmitic acid (PA)-treated hepatocytes, GADD45β deficiency exacerbated lipid accumulation and upregulated lipogenic genes (SREBP1, FASN, ACC). Mechanistically, GADD45β directly bound to SIRT1 and inhibited its ubiquitination, thereby prolonging SIRT1 protein stability. Enhanced SIRT1 stability increased AMPK phosphorylation, which suppressed SREBP1-mediated transcription of lipogenic targets. Crucially, hepatic overexpression of GADD45β reversed PA-induced steatosis in vitro. Our study uncovered a GADD45β/SIRT1-/AMPK axis as a central regulator of hepatic lipogenesis, proposing GADD45β as a therapeutic target for MASLD.

Indexed as

AMP-Activated Protein KinasesLipogenesisLiverSirtuin 1Sterol Regulatory Element Binding Protein 1AnimalsAntigens, DifferentiationFatty LiverGADD45 ProteinsHepatocytesHumansMaleMiceMice, Inbred C57BLProteolysisSignal TransductionAMP-Activated Protein KinasesAntigens, DifferentiationGadd45b protein, mouseGADD45 ProteinsSirt1 protein, mouseSirtuin 1Srebf1 protein, mouseSterol Regulatory Element Binding Protein 1GADD45βLipogenesisMASLDSIRT1Ubiquitination

Identifiers

PMID41203689
PMCPMC12594973

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Registered trials

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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.