Evidence map›Paper›PMID 24703845›Full record

ArticleCell reports2014

Macrophage CGI-58 deficiency activates ROS-inflammasome pathway to promote insulin resistance in mice.

Hongming Miao, Juanjuan Ou, Yinyan Ma, Feng Guo, Zhenggang Yang, Melvin Wiggins, Chaohong Liu, Wenxia Song, Xianlin Han, Miao Wang and 8 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Identification of immune-related hub genes in spinal cord injury.European journal of medical research · 2024
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

1 more citing papers are in PubMed but not listed here.

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

18 authors at 6 institutions in 2 countries.

Hongming MiaoDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA; Department of Biochemistry and Molecular Biology, The Third Military Medical University, Chongqing 400038, China.
Juanjuan OuDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA; Department of Oncology, Southwest Hospital, The Third Military Medical University, Chongqing 400038, China.
Yinyan MaDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA.
Feng GuoDepartment of Biochemistry, Wake Forest University Health Sciences, Winston-Salem, NC 27157, USA.
Zhenggang YangDepartment of Internal Medicine, Wake Forest University Health Sciences, Winston-Salem, NC 27157, USA.
Melvin WigginsDepartment of Cell Biology & Molecular Genetics, University of Maryland, College Park, MD 20742, USA.
Chaohong LiuDepartment of Cell Biology & Molecular Genetics, University of Maryland, College Park, MD 20742, USA.
Wenxia SongDepartment of Cell Biology & Molecular Genetics, University of Maryland, College Park, MD 20742, USA.
Xianlin HanDiabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827, USA.
Miao WangDiabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, Orlando, FL 32827, USA.
Qiang CaoDepartment of Biology, Georgia State University, Atlanta, GA 30303, USA.
Bik-Ho Florence ChungDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA.
Dan YangDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA.
Houjie LiangDepartment of Oncology, Southwest Hospital, The Third Military Medical University, Chongqing 400038, China.
Bingzhong XueDepartment of Biology, Georgia State University, Atlanta, GA 30303, USA.
Hang ShiDepartment of Biology, Georgia State University, Atlanta, GA 30303, USA.
Lixia GanDepartment of Biochemistry and Molecular Biology, The Third Military Medical University, Chongqing 400038, China. Electronic address: ganlixia@yahoo.com.
Liqing YuDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA. Electronic address: lyu123@umd.edu.
University of Maryland, College Park · USGeorgia State University · USSanford Burnham Prebys Medical Discovery Institute · USSouthwest Hospital · CNWake Forest University · USArmy Medical University · CN

Funding

Research BaseP30DK072488 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI MITCHELL, BRAXTON D, TAYLOR, SIMEON I. · 2005 to 2019
$17.3M
Macrophage AMPK, Inflammation, and AtherosclerosisR01HL107500 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI XUE, BINGZHONG · 2012 to 2016
$1.8M
NPC1L1 and Metabolic DiseasesR01DK085176 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI YU, LIQING · 2010 to 2014
$1.6M
The AMP-Activated Protein Kinase (AMPK) Antagonizes Inflammation Through SIRT1R01DK084172 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SHI, HANG · 2009 to 2012
$1.2M
NHLBI NIH HHS R01 HL107500NHLBI NIH HHS R01HL107500NIDDK NIH HHS P30 DK072488NIDDK NIH HHS R01 DK084172NIDDK NIH HHS R01DK084172NIDDK NIH HHS R01 DK085176NIDDK NIH HHS R01DK085176
6 · The paper itself

Abstract

Overnutrition activates a proinflammatory program in macrophages to induce insulin resistance (IR), but its molecular mechanisms remain incompletely understood. Here, we show that saturated fatty acid and lipopolysaccharide, two factors implicated in high-fat diet (HFD)-induced IR, suppress macrophage CGI-58 expression. Macrophage-specific CGI-58 knockout (MaKO) in mice aggravates HFD-induced glucose intolerance and IR, which is associated with augmented systemic/tissue inflammation and proinflammatory activation of adipose tissue macrophages. CGI-58-deficient macrophages exhibit mitochondrial dysfunction due to defective peroxisome proliferator-activated receptor (PPAR)γ signaling. Consequently, they overproduce reactive oxygen species (ROS) to potentiate secretion of proinflammatory cytokines by activating NLRP3 inflammasome. Anti-ROS treatment or NLRP3 silencing prevents CGI-58-deficient macrophages from oversecreting proinflammatory cytokines and from inducing proinflammatory signaling and IR in the cocultured fat slices. Anti-ROS treatment also prevents exacerbation of inflammation and IR in HFD-fed MaKO mice. Our data thus establish CGI-58 as a suppressor of overnutrition-induced NLRP3 inflammasome activation in macrophages.

Indexed as

1-Acylglycerol-3-Phosphate O-AcyltransferaseAnimalsCarrier ProteinsDown-RegulationFatty AcidsInflammasomesInsulin ResistanceLipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen Species1-Acylglycerol-3-Phosphate O-AcyltransferaseABHD5 protein, humanAbhd5 protein, mouseCarrier ProteinsFatty AcidsInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen Species

Identifiers

PMID24703845
PMCPMC4040312
OpenAlexW2086635120

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.