Evidence map›Paper›PMID 35447114›Full record

ArticleThe Journal of biological chemistry2022

Leukemia inhibitory factor protects against liver steatosis in nonalcoholic fatty liver disease patients and obese mice.

Youwen Yuan, Kangli Li, Fei Teng, Weiwei Wang, Bing Zhou, Xuan Zhou, Jiayang Lin, Xueru Ye, Yajuan Deng, Wenhui Liu and 7 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. [Two-sample Mendelian randomization analysis for the causal relationship between 91 circulating inflammatory proteins and liver cirrhosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
  4. Article
  5. Review
  6. Leukemia inhibitory factor (LIF) receptor amplifies pathogenic activation of fibroblasts in lung fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Article
  9. CLCF1 inhibits energy expenditure via suppressing brown fat thermogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Comparative Proteomic Analysis of Liver Tissues and Serum inInternational journal of molecular sciences · 2022
    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

17 authors at 4 institutions in 1 country.

Youwen YuanDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Kangli LiDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Fei TengDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Weiwei WangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Bing ZhouThe Key Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China.
Xuan ZhouDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jiayang LinDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xueru YeDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yajuan DengDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wenhui LiuDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Shenjian LuoDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Peizhen ZhangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Deying LiuDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Minghua ZhengMAFLD Research Center, Department of Hepatology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China; Key Laboratory of Diagnosis and Treatment for The Development of Chronic Liver Disease, Zhejiang Province, Wenzhou, Zhejiang, China.
Jin LiDivision of Endocrinology, Department of Medicine, Shanxi Medical University affiliated Second Hospital, Taiyuan, China.
Yan LuThe Key Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address: lu.yan2@zs-hospital.sh.cn.
Huijie ZhangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China. Electronic address: huijiezhang2005@126.com.
Nanfang Hospital · CNFudan University · CNShanxi Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases worldwide. However, the molecular mechanisms that promote dysregulation of hepatic triglyceride metabolism and lead to NAFLD are poorly understood, and effective treatments are limited. Leukemia inhibitory factor (LIF) is a member of the interleukin-6 cytokine family and has been shown to regulate a variety of physiological processes, although its role in hepatic triglyceride metabolism remains unknown. In the present study, we measured circulating LIF levels by ELISA in 214 patients with biopsy-diagnosed NAFLD as well as 314 normal control patients. We further investigated the potential role and mechanism of LIF on hepatic lipid metabolism in obese mice. We found that circulating LIF levels correlated with the severity of liver steatosis. Patients with ballooning, fibrosis, lobular inflammation, and abnormally elevated liver injury markers alanine transaminase and aspartate aminotransferase also had higher levels of serum LIF than control patients. Furthermore, animal studies showed that white adipose tissue-derived LIF could ameliorate liver steatosis through activation of hepatic LIF receptor signaling pathways. Together, our results suggested that targeting LIF-LIF receptor signaling might be a promising strategy for treating NAFLD.

Indexed as

Non-alcoholic Fatty Liver DiseaseAnimalsHumansLeukemia Inhibitory FactorLiverMiceMice, ObeseTriglyceridesLeukemia Inhibitory FactorTriglyceridesLIFLIFRlipogenesisnonalcoholic fatty liver diseaseobesity

Identifiers

PMID35447114
PMCPMC9123280
OpenAlexW4223943508

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.