Evidence map›Paper›PMID 26754764›Full record

ReviewImmunologic research2016

The role of complement system in adipose tissue-related inflammation.

Sonia I Vlaicu, Alexandru Tatomir, Dallas Boodhoo, Stefan Vesa, Petru A Mircea, Horea Rus

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Is the endotoxin-complement cascade the major driver in lipedema?Trends in endocrinology and metabolism: TEM · 2024
    Review
  8. Article
  9. Nutrients · 2023
    Article
  10. Deletion of complement factor 5 amplifies glucose intolerance in obese male but not female mice.American journal of physiology. Endocrinology and metabolism · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 2 countries.

Sonia I VlaicuDepartment of Neurology, University of Maryland, School of Medicine, 655 W Baltimore St, BRB 12-033, Baltimore, MD, 21201, USA.
Alexandru TatomirDepartment of Neurology, University of Maryland, School of Medicine, 655 W Baltimore St, BRB 12-033, Baltimore, MD, 21201, USA.
Dallas BoodhooDepartment of Neurology, University of Maryland, School of Medicine, 655 W Baltimore St, BRB 12-033, Baltimore, MD, 21201, USA.
Stefan VesaDepartment of Pharmacology, Toxicology and Clinical Pharmacology, "Iuliu Haţieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Petru A MirceaDepartment of Internal Medicine, "Iuliu Haţieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Horea RusDepartment of Neurology, University of Maryland, School of Medicine, 655 W Baltimore St, BRB 12-033, Baltimore, MD, 21201, USA. hrus@umaryland.edu.
Iuliu Hațieganu University of Medicine and Pharmacy · ROVA Maryland Health Care System · USUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the common factor linking adipose tissue to the metabolic context of obesity, insulin resistance and atherosclerosis are associated with a low-grade chronic inflammatory status, to which the complement system is an important contributor. Adipose tissue synthesizes complement proteins and is a target of complement activation. C3a-desArg/acylation-stimulating protein stimulates lipogenesis and affects lipid metabolism. The C3a receptor and C5aR are involved in the development of adipocytes' insulin resistance through macrophage infiltration and the activation of adipose tissue. The terminal complement pathway has been found to be instrumental in promoting hyperglycemia-associated tissue damage, which is characteristic of the major vascular complications of diabetes mellitus and diabetic ketoacidosis. As a mediator of the effects of the terminal complement complex C5b-9, RGC-32 has an impact on energy expenditure as well as lipid and glucose metabolic homeostasis. All of this evidence, taken together, indicates an important role for complement activation in metabolic diseases.

Indexed as

Insulin ResistanceAdipose TissueAnimalsComplement ActivationComplement System ProteinsEnergy MetabolismHumansInflammationLipid MetabolismObesityComplement System ProteinsAdipose tissueC5b-9Complement activationDiabetes mellitusMetabolic syndromeRGC-32

Identifiers

PMID26754764
OpenAlexW2289584262

What OpenQuestion holds

Textmetadata
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.