Evidence map›Paper›PMID 39612121›Full record

ReviewCurrent hypertension reports2024

Targeting the Brain Leptin-Melanocortin Pathway to Treat Heart Failure.

Ana C M Omoto, Jussara M do Carmo, Alan J Mouton, Zhen Wang, Xuan Li, Robert Spitz, John E Hall, Alexandre A da Silva

Abstract readReview
In one paragraph

Review in Current hypertension reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. The Synthetic Melanocortin Agonist NDP-MSH Ameliorates THSD7A-Associated Membranous Nephropathy in an Active Immunization Mouse Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. 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

8 authors.

Ana C M OmotoDepartment of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA. aomoto@umc.edu.
Jussara M do CarmoDepartment of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.
Alan J MoutonDepartment of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.
Zhen WangDepartment of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.
Xuan LiDepartment of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.
Robert SpitzDepartment of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.
John E HallDepartment of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.
Alexandre A da SilvaDepartment of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.

Funding

Tracking and Evaluation CoreU54GM115428 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI GOMEZ-SANCHEZ, CELSO ENRIQUE · 2016 to 2025
$38.2M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI HALL, JOHN E · 2013 to 2022
$23.4M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
Pilot Projects ProgramP30GM149404 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI John E Hall · 2023 to 2026
$6.3M
Anti-Inflammatory Roles and Macrophage Metabolism of Lactate and Ketones during Myocardial InfarctionR01HL166737 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Alan J Mouton · 2023 to 2026
$2.4M
Cardiac protective mechanisms of melanocortin system activationR01HL163076 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Jussara M. Do Carmo, Alexandre Alves da Silva · 2023 to 2026
$2.3M
American Heart Association Postdoctoral Fellowship Award AHA POST835218NHLBI NIH HHS 1R01HL163076NHLBI NIH HHS R01 HL163076NHLBI NIH HHS R01 HL166737NHLBI NIH HHS T32 HL105324NIGMS NIH HHS P20 GM104357NIGMS NIH HHS P20GM104357, P30GM149404 and U54 GM115428NIGMS NIH HHS P30 GM149404NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

purpose of the reviewThe role of leptin in regulating cardiac function is still controversial with conflicting results in clinical and preclinical studies. However, most previous studies have not considered leptin's powerful cardiac effects that are mediated via activation of central nervous system (CNS) leptin receptors (LepRs) which, in turn, elicit major improvements in cardiac metabolism. In this review, we focus mainly on the role of leptin in regulating cardiac function via its CNS LepRs and downstream signaling pathways, such as the brain melanocortin system. RECENT

findingsStudies from our laboratory showed that CNS LepR activation, without raising plasma leptin levels, has remarkable beneficial effects on cardiac metabolism and function that protect the heart during pathological conditions, including heart failure (HF) induced by myocardial infarction (MI). These cardioprotective effects of leptin appear to be mediated by stimulation of CNS proopiomelanocortin neurons and subsequent activation of melanocortin 4 receptors (MC4R) in the brain. Chronic activation of the brain leptin-melanocortin pathway improves cardiac function and metabolism following myocardial infarction. However, the mechanism underlying this brain-heart crosstalk remains unclear and may have important implications for the development of new therapies for MI and HF.

Indexed as

BrainHeart FailureLeptinMelanocortinsReceptors, LeptinSignal TransductionAnimalsHumansMyocardial InfarctionReceptor, Melanocortin, Type 4LeptinMelanocortinsReceptor, Melanocortin, Type 4Receptors, LeptinCentral nervous systemLeptin receptorsMelanocortin 4 receptors (MC4R)Myocardial infarction

Identifiers

PMID39612121
PMCPMC11607000

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.