Evidence map›Paper›PMID 30681731›Full record

ArticleHepatology (Baltimore, Md.)2019

Adipocyte Death Preferentially Induces Liver Injury and Inflammation Through the Activation of Chemokine (C-C Motif) Receptor 2-Positive Macrophages and Lipolysis.

Seung-Jin Kim, Dechun Feng, Adrien Guillot, Shen Dai, Fengming Liu, Seonghwan Hwang, Richard Parker, Wonhyo Seo, Yong He, Grzegorz Godlewski and 5 more

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

48 citing papers in PubMed, 76 citations in OpenAlex.

  1. Hepatic steatosis affects the outcome of anti-tuberculosis treatment in pulmonary tuberculosis patients.Journal of clinical tuberculosis and other mycobacterial diseases · 2026
    Article
  2. Review
  3. Anti-Obesity Effects of Pear Extract (International journal of stem cells · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 2025
    Review
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  10. Article
  11. Review
  12. Article
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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 at 4 institutions in 3 countries.

Seung-Jin KimLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Dechun FengLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Adrien GuillotLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Shen DaiDepartment of Neuroscience, School of Medicine, Temple University, Philadelphia, PA.
Fengming LiuDepartment of Neuroscience, School of Medicine, Temple University, Philadelphia, PA.
Seonghwan HwangLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Richard ParkerLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Wonhyo SeoLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Yong HeLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Grzegorz GodlewskiLaboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Won-Il JeongLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Yuhong LinLaboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Xuebin QinDepartment of Neuroscience, School of Medicine, Temple University, Philadelphia, PA.
George KunosLaboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
Bin GaoLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD.
National Institute on Alcohol Abuse and Alcoholism · USNational Institutes of Health · USTemple University · USKorea Advanced Institute of Science and Technology · KR

Funding

Endocannabinoids And Energy HomeostasisZIAAA000350 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI KUNOS, GEORGE · 2009 to 2025
$28.4M
Pathogenesis and Novel Therapeutic Targets of Steatotic Liver Disease and CancerZIAAA000369 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI GAO, BIN · 2009 to 2025
$23.4M
Molecular mechanisms of liver injury, repair, and immunityZIAAA000368 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI GAO, BIN · 2009 to 2023
$16.1M
Role of caspase-1 activation in HIV-1 associated atherogenesisR01HL141132 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI BURDO, TRICIA HELEN, QIN, XUEBIN · 2018 to 2021
$2.5M
Atherogenic roles of complement systemR01HL130233 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI QIN, XUEBIN, WANG, HONG · 2016 to 2019
$2.5M
Generation and Characterization of a Novel Cell Subpopulation Ablation ModelR21OD024931 · OD · TULANE UNIVERSITY OF LOUISIANA · PI QIN, XUEBIN · 2018 to 2019
$450k
Intramural NIH HHS ZIA AA000368Intramural NIH HHS ZIA AA000369Medical Research Council G1100448NHLBI NIH HHS R01 HL130233NHLBI NIH HHS R01 HL141132NIAAANIH HHS R01 HL130233NIH HHS R21 OD024931
6 · The paper itself

Abstract

Adipocyte death occurs under various physiopathological conditions, including obesity and alcohol drinking, and can trigger organ damage particularly in the liver, but the underlying mechanisms remain obscure. To explore these mechanisms, we developed a mouse model of inducible adipocyte death by overexpressing the human CD59 (hCD59) on adipocytes (adipocyte-specific hCD59 transgenic mice). Injection of these mice with intermedilysin (ILY), which rapidly lyses hCD59 expressing cells exclusively by binding to the hCD59 but not mouse CD59, resulted in the acute selective death of adipocytes, adipose macrophage infiltration, and elevation of serum free fatty acid (FFA) levels. ILY injection also resulted in the secondary damage to multiple organs with the strongest injury observed in the liver, with inflammation and hepatic macrophage activation. Mechanistically, acute adipocyte death elevated epinephrine and norepinephrine levels and activated lipolysis pathways in adipose tissue in a chemokine (C-C motif) receptor 2-positive (CCR2

Indexed as

AdipocytesAdipose TissueAnimalsBacteriocinsCell DeathDisease Models, AnimalEpinephrineFatty Acids, NonesterifiedFemaleInflammationIsoproterenolLipolysisLiver DiseasesMacrophagesMaleMice, TransgenicBacteriocinsCcr2 protein, mouseEpinephrineFatty Acids, Nonesterifiedintermedilysin protein, Streptococcus intermediusIsoproterenolNorepinephrineReceptors, CCR2

Identifiers

PMID30681731
PMCPMC6461506
OpenAlexW2911229126

What OpenQuestion holds

Textmetadata
LicenceTDM
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.