Evidence map›Paper›PMID 35742928›Full record

ArticleInternational journal of molecular sciences2022

SOCS3 Ablation in Leptin Receptor-Expressing Cells Causes Autonomic and Cardiac Dysfunctions in Middle-Aged Mice despite Improving Energy and Glucose Metabolism.

João A B Pedroso, Ivson B da Silva, Thais T Zampieri, Leonardo T Totola, Thiago S Moreira, Ana P T Taniguti, Gabriela P Diniz, Maria Luiza M Barreto-Chaves, Jose Donato

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026
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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

9 authors at 2 institutions in 1 country.

João A B PedrosoDepartamento de Fisiologia e Biofisica, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-000, Brazil.
Ivson B da SilvaDepartamento de Anatomia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-900, Brazil.
Thais T ZampieriDepartamento de Fisiologia e Biofisica, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-000, Brazil.
Leonardo T TotolaDepartamento de Fisiologia e Biofisica, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-000, Brazil.
Thiago S MoreiraDepartamento de Fisiologia e Biofisica, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-000, Brazil.
Ana P T TanigutiDepartamento de Anatomia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-900, Brazil.
Gabriela P DinizDepartamento de Anatomia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-900, Brazil.ORCID 0000-0003-1278-4431
Maria Luiza M Barreto-ChavesDepartamento de Anatomia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-900, Brazil.ORCID 0000-0001-5514-7921
Jose DonatoDepartamento de Fisiologia e Biofisica, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo 05508-000, Brazil.ORCID 0000-0002-4166-7608
Universidade de São Paulo · BRUniversidade Federal da Paraíba · BR

Funding

São Paulo Research Foundation 2013/25032-2; 2011/12893-4; 2013/04703-6; 2012/15517-6; 2010/18086-0 and 2020/01318/8
6 · The paper itself

Abstract

Leptin resistance is a hallmark of obesity. Treatments aiming to improve leptin sensitivity are considered a promising therapeutical approach against obesity. However, leptin receptor (LepR) signaling also modulates several neurovegetative aspects, such as the cardiovascular system and hepatic gluconeogenesis. Thus, we investigated the long-term consequences of increased leptin sensitivity, considering the potential beneficial and deleterious effects. To generate a mouse model with increased leptin sensitivity, the suppressor of cytokine signaling 3 (SOCS3) was ablated in LepR-expressing cells (LepR

Indexed as

Heart DiseasesReceptors, LeptinAnimalsEnergy MetabolismGlucoseLeptinMiceNeuronsObesitySuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsGlucoseLeptinReceptors, LeptinSocs3 protein, mouseSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteinsagingcardiovascular systemhearthypothalamusleptinobesity

Identifiers

PMID35742928
PMCPMC9223472
OpenAlexW4281715288

What Socratic 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 Socratic graph.