Evidence map›Paper›PMID 42212316›Full record

ArticleInternational journal of biological sciences2026

CXCL6 exacerbates metabolic dysfunction-associated steatohepatitis by suppressing LPIN1-mediated fatty acid oxidation in hepatocytes.

Ye Eun Cho, Min-Ju Kim, Yeonsoo Kim, Hyeokjin Lim, Yunseo Park, Sangok Kim, Seung-Jin Kim, Jin-Wook Yoo, Seungjin Ryu, Parkyong Song and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 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
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

15 authors.

Ye Eun ChoCollege of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 46241, Republic of Korea.
Min-Ju KimCollege of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 46241, Republic of Korea.
Yeonsoo KimCollege of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 46241, Republic of Korea.
Hyeokjin LimCollege of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 46241, Republic of Korea.
Yunseo ParkCollege of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 46241, Republic of Korea.
Sangok KimKorea Bioinformation Center, Korea Research Institute of Bioscience & Biotechnology, Daejeon 34141, Republic of Korea.
Seung-Jin KimDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon 24341, Republic of Korea.
Jin-Wook YooCollege of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 46241, Republic of Korea.
Seungjin RyuDepartment of Biochemistry, Chung-Ang University College of Medicine, Seoul 06974, Republic of Korea.
Parkyong SongDepartment of Convergence Medicine, Pusan National University School of Medicine, Yangsan 50612, Republic of Korea.
Changwan HongDepartment of Anatomy, Pusan National University School of Medicine, Yangsan 50612, Republic of Korea.
Yong HeState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai 201203, China.
Haeseung LeeCollege of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 46241, Republic of Korea.
Je-Yoel ChoDepartment of Biochemistry, Brain Korea 21 Project and Research Institute for Veterinary Science, Seoul National University, College of Veterinary Medicine, Seoul 08826, Republic of Korea.
Seonghwan HwangCollege of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan 46241, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progression of hepatic steatosis to metabolic dysfunction-associated steatohepatitis (MASH) is driven by impaired fatty acid (FA) oxidation and subsequent hepatocyte lipotoxicity. While MASH is characterized by upregulation of the neutrophil chemoattractant CXCL6, which functions through CXCR2, the direct impact of this pathway on hepatocyte FA metabolism during MASH progression remains unclear. Here, we demonstrate that hepatic overexpression of

Indexed as

Chemokine CXCL6Fatty AcidsFatty LiverHepatocytesPhosphatidate PhosphataseAnimalsChemokine CXCL5HumansMaleMiceMice, Inbred C57BLOxidation-ReductionChemokine CXCL5Chemokine CXCL6Fatty AcidsPhosphatidate Phosphatasechemokinefatty acid oxidationhepatocytelipotoxicitysteatosis

Identifiers

PMID42212316
PMCPMC13215063

What OpenQuestion holds

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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 OpenQuestion graph.