Evidence map›Paper›PMID 32824322›Full record

ReviewInternational journal of molecular sciences2020

Role of Leptin in Inflammation and Vice Versa.

Antonio Pérez-Pérez, Flora Sánchez-Jiménez, Teresa Vilariño-García, Víctor Sánchez-Margalet

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 4 pooled it
14.5field-weighted citation impact, top 1% 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

180 citing papers in PubMed, 4 syntheses or guidelines pooled it, 312 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Review
  12. Investigating the Role ofJournal of clinical research in pediatric endocrinology · 2026
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

120 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

4 authors at 1 institution in 1 country.

Antonio Pérez-PérezDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Virgen Macarena University Hospital, University of Seville, 41009 Seville, Spain.ORCID 0000-0002-5660-735X
Flora Sánchez-JiménezDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Virgen Macarena University Hospital, University of Seville, 41009 Seville, Spain.
Teresa Vilariño-GarcíaDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Virgen Macarena University Hospital, University of Seville, 41009 Seville, Spain.
Víctor Sánchez-MargaletDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Virgen Macarena University Hospital, University of Seville, 41009 Seville, Spain.ORCID 0000-0001-8638-8680
Hospital Universitario Virgen Macarena · ES

Funding

Instituto de Salud Carlos III PI19/01741
6 · The paper itself

Abstract

Inflammation is an essential immune response for the maintenance of tissue homeostasis. In a general sense, acute and chronic inflammation are different types of adaptive response that are called into action when other homeostatic mechanisms are insufficient. Although considerable progress has been made in understanding the cellular and molecular events that are involved in the acute inflammatory response to infection and tissue injury, the causes and mechanisms of systemic chronic inflammation are much less known. The pathogenic capacity of this type of inflammation is puzzling and represents a common link of the multifactorial diseases, such as cardiovascular diseases and type 2 diabetes. In recent years, interest has been raised by the discovery of novel mediators of inflammation, such as microRNAs and adipokines, with different effects on target tissues. In the present review, we discuss the data emerged from research of leptin in obesity as an inflammatory mediator sustaining multifactorial diseases and how this knowledge could be instrumental in the design of leptin-based manipulation strategies to help restoration of abnormal immune responses. On the other direction, chronic inflammation, either from autoimmune or infectious diseases, or impaired microbiota (dysbiosis) may impair the leptin response inducing resistance to the weight control, and therefore it may be a cause of obesity. Thus, we are reviewing the published data regarding the role of leptin in inflammation, and the other way around, the role of inflammation on the development of leptin resistance and obesity.

Indexed as

Adaptive ImmunityAnimalsAutoimmune DiseasesCommunicable DiseasesHumansImmunity, InnateLeptinObesityLeptininflammationleptinleptin resistancemicrobiotaobesity

Identifiers

PMID32824322
PMCPMC7460646
OpenAlexW3049167578

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.