Evidence map›Paper›PMID 39731358›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Hepatocyte-Derived FGF1 Alleviates Isoniazid and Rifampicin-Induced Liver Injury by Regulating HNF4α-Mediated Bile Acids Synthesis.

Qian Lin, Jiaren Zhang, Jie Qi, Jialin Tong, Shenghuan Chen, Sudan Zhang, Xingru Liu, Huatong Lou, Jiaxuan Lv, Ruoyu Lin and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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. FGF family in health and disease.Molecular biomedicine · 2026
    Review
  4. Human FGF1Cells · 2026
    Article
  5. Article
  6. Article
  7. Frontiers in microbiology · 2025
    Article
  8. Article
  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

16 authors.

Qian LinSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jiaren ZhangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jie QiSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jialin TongSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Shenghuan ChenSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Sudan ZhangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Xingru LiuSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Huatong LouSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jiaxuan LvSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Ruoyu LinSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Junjun XieDepartment of Pharmacy, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310016, China.
Yi JinDepartment of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Yang WangSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Lei YingSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jiamin WuSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jianlou NiuSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.ORCID https://orcid.org/0000-0001-7913-4885

Funding

Natural Science Foundation of China 82273996Natural Science Foundation of Zhejiang Province LTGY24H030011Natural Science Foundation of Zhejiang Province LY21G300004Natural Science Foundation of Zhejiang Province LYY22H310001
6 · The paper itself

Abstract

Isoniazid and rifampicin co-therapy are the main causes of anti-tuberculosis drug-induced liver injury (ATB-DILI) and acute liver failure, seriously threatening human health. However, its pathophysiology is not fully elucidated. Growing evidences have shown that fibroblast growth factors (FGFs) play a critical role in diverse aspects of liver pathophysiology. The aim of this study is to investigate the role of FGFs in the pathogenesis of isoniazid (INH) and rifampicin (RIF)-induced liver injury. Through systematic screening, this study finds that hepatic FGF1 expression is significantly downregulated in both mouse model and human patients challenged with INH and RIF. Hepatocyte-specific Fgf1 deficiency exacerbates INH and RIF-induced liver injury resulted from elevated bile acids (BAs) synthases and aberrant BAs accumulation. Conversely, pharmacological administration of the non-mitogenic FGF1 analog - FGF1

Indexed as

Bile Acids and SaltsChemical and Drug Induced Liver InjuryFibroblast Growth Factor 1Hepatocyte Nuclear Factor 4HepatocytesIsoniazidRifampinAnimalsAntitubercular AgentsDisease Models, AnimalHumansLiverMaleMiceMice, Inbred C57BLAntitubercular AgentsBile Acids and SaltsFibroblast Growth Factor 1Hepatocyte Nuclear Factor 4IsoniazidRifampinanti‐tuberculosis drug‐induced liver injurybile acids biosynthesisFGFR4Fibroblast growth factorsHNF4α

Identifiers

PMID39731358
PMCPMC11831436

What Socratic 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 Socratic graph.