Evidence map›Paper›PMID 40019662›Full record

ReviewNeuromolecular medicine2025

Leptin and Leptin Signaling in Multiple Sclerosis: A Narrative Review.

Juan Antonio Flores-Cordero, Amalia Aranaz-Murillo, Teresa Vilariño-García, Antonio Pérez-Pérez, Guillermo Izquierdo, Rocío Flores-Campos, Lourdes Hontecillas-Prieto, Daniel J García-Domínguez, Víctor Sánchez-Margalet

Abstract readReview
In one paragraph

Review in Neuromolecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

9 authors.

Juan Antonio Flores-Cordero *Department of Medical Biochemistry and Molecular Biology, and Immunology, Medical School, University of Seville, Seville, Spain.
Amalia Aranaz-Murillo *Department of Medical Biochemistry and Molecular Biology, and Immunology, Medical School, University of Seville, Seville, Spain.
Teresa Vilariño-GarcíaDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical School, Virgen del Rocio University Hospital, Seville, Spain.
Antonio Pérez-PérezDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical School, University of Seville, Seville, Spain.
Guillermo IzquierdoNeurology Service, Virgen Macarena University Hospital, University of Seville, Seville, Spain.
Rocío Flores-CamposDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical School, University of Seville, Seville, Spain.
Lourdes Hontecillas-PrietoDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical School, University of Seville, Seville, Spain.
Daniel J García-DomínguezDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical School, University of Seville, Seville, Spain.
Víctor Sánchez-MargaletDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical School, University of Seville, Seville, Spain. margalet@us.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity, a pandemic health problem, is now considered as a chronic inflammatory state, related to many autoimmune diseases, such as multiple sclerosis. Thus, adipokines, inflammatory mediators secreted by adipose tissue, play an important role modulating the immune response. In this context, obesity, especially during adolescent age, seems to be a key factor for the development of multiple sclerosis. Leptin, the main pro-inflammatory adipokine secreted by the adipose tissue, has been found increased in patients with multiple sclerosis and is able to regulate the immune system promoting a pro-inflammatory response. Leptin signaling in both innate and adaptative immune cells might have immunomodulatory effects in the context of multiple sclerosis. In this way, leptin has been found to produce a Th1 and Th17 response, increasing M1 macrophages and decreasing regulatory T cells and Th2 response. Moreover, circulating inflammatory adipokines, such as leptin, have been found in people with multiple sclerosis. In the present work, we are reviewing literature to update the body of knowledge regarding the role of obesity and leptin in multiple sclerosis.

Indexed as

LeptinMultiple SclerosisSignal TransductionAdipose TissueAnimalsCytokinesHumansMacrophagesObesityReceptors, LeptinTh17 CellsTh1 CellsCytokinesLEP protein, humanLeptinReceptors, LeptinInflammationLeptinMultiple SclerosisObesity

Identifiers

PMID40019662
PMCPMC11870953

What OpenQuestion holds

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Registered trials

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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.