Evidence mapPaperPMID 40730679Full record

ArticleCommunications biology2025

Pantothenic acid ameliorates hepatic fibrosis by targeting IGFBP6 to regulate the TGF-β/SMADs pathway.

Zhengxin Jin, Zhengsen Jin, Zeyu Liu, Yongcheng Yin, Yuchen Zhang, Ying Zhang, Jianning Kang, Yuepeng Fang, Wei Jiang, Bin Ning

Abstract read
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Pantothenic Acid Derivatives Modulate Oxidative Stress and Hepatic Fibrosis in Bile Duct Ligation-Induced Cholestatic Liver Injury.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
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.

Zhengxin JinJinan Central Hospital, Shandong University, No.105, Jiefang Road, Jinan, Shandong, China.
Zhengsen JinDepartment of Clinical Pharmacology of Traditional Chinese Medicine, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Zeyu LiuCentral Hospital Affiliated to Shandong First Medical University, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Yongcheng YinCentral Hospital Affiliated to Shandong First Medical University, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Yuchen ZhangCentral Hospital Affiliated to Shandong First Medical University, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Ying ZhangCentral Hospital Affiliated to Shandong First Medical University, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Jianning KangJinan Central Hospital, Shandong University, No.105, Jiefang Road, Jinan, Shandong, China.
Yuepeng FangJinan Central Hospital, Shandong University, No.105, Jiefang Road, Jinan, Shandong, China.
Wei JiangCentral Hospital Affiliated to Shandong First Medical University, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Bin NingJinan Central Hospital, Shandong University, No.105, Jiefang Road, Jinan, Shandong, China. ningbin@sdu.edu.cn.ORCID http://orcid.org/0000-0002-7592-9485

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82071383
6 · The paper itself

Abstract

Hepatic fibrosis progression involves complex multicellular crosstalk, highlighting the critical need to identify key therapeutic targets. In this study, we identify insulin-like growth factor binding protein 6 (IGFBP6) as a marker specifically enriched in hepatic stellate cells (HSCs) and upregulated in viral hepatitis-associated fibrosis. Using thioacetamide (TAA)-induced mouse models and transforming growth factor-β (TGF-β)-stimulated cell models, we demonstrate the pro-fibrotic role of IGFBP6. Through network pharmacology screening, pantothenic acid (PA) is identified as a potent compound targeting IGFBP6. PA administration significantly reduces collagen deposition, attenuates HSCs' activation, and decreases hepatic fibrosis-related markers. Notably, PA maintains efficacy in mouse models with established fibrosis. Mechanistically, PA directly interacts with IGFBP6, inducing ubiquitin-dependent degradation and inhibiting TGF-β/SMADs signaling. This study identifies IGFBP6 as a driver of hepatic fibrosis and validates PA as a potent therapeutic agent. Therefore, targeting IGFBP6 with PA offers a potential clinical treatment strategy for hepatic fibrosis.

Indexed as

Insulin-Like Growth Factor Binding ProteinsLiver CirrhosisPantothenic AcidSignal TransductionSmad ProteinsTransforming Growth Factor betaAnimalsDisease Models, AnimalHepatic Stellate CellsHumansMaleMiceMice, Inbred C57BLinsulin-like growth factor binding protein-related protein 1Insulin-Like Growth Factor Binding ProteinsPantothenic AcidSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID40730679
PMCPMC12307719

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.