Evidence map›Paper›PMID 41281741›Full record

ArticleInternational journal of biological sciences2025

GDF10 attenuates MASH progression by restoring quiescent hepatic stellate cells via competitive inhibition of TGF-β/SMAD2 signaling.

Yajie Peng, Hongyan Lei, Jiahui Zhao, Huajuan Wang, Zheng Luo, Dixin Wang, Shujun Shi, Tianyi Wang, Jin Li, Zhiqing Pang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

12 authors.

Yajie PengMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Hongyan LeiMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Jiahui ZhaoMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Huajuan WangMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Zheng LuoMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Dixin WangMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Shujun ShiMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Tianyi WangMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Jin LiState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, 200438, Shanghai, China.
Zhiqing PangKey Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, 201203, Shanghai, China.
Bo WangMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.
Xuelian XiongMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 200020, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis has emerged as the primary determinant of outcomes in metabolic dysfunction-associated steatohepatitis (MASH). Quiescent hepatic stellate cells (HSCs) differentiate into activated HSCs or myofibroblasts, which drives liver fibrosis and contribute to the progressive loss of hepatic function. MASH with progressive fibrosis lacks effective therapies due to incomplete understanding of HSCs regulation. Here, we identify growth differentiation factor 10 (GDF10) as a master regulator of HSCs quiescence that ameliorates fibrosis through shifting HSC functions to restore HSC balance of transcriptional and metabolic reprogramming. Single-cell RNA sequencing revealed HSC-specific

Indexed as

Fatty LiverGrowth Differentiation Factor 10Hepatic Stellate CellsSmad2 ProteinTransforming Growth Factor betaAnimalsHumansLiver CirrhosisMaleMiceMice, Inbred C57BLSignal TransductionGrowth Differentiation Factor 10Smad2 ProteinTransforming Growth Factor betaGDF10HSCsliver fibrosisMASH

Identifiers

PMID41281741
PMCPMC12631229

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.