Evidence map›Paper›PMID 41793552›Full record

ArticleMolecular biology reports2026

Genetic deletion of MrgD receptor disrupts cardiac protein homeostasis in mice.

Beatriz Alexandre-Santos, Luiza Mazzali Ferraz, Ana Beatriz Proença, Nícia Pedreira Soares, Guilherme Dos Santos Reis, Maria Eduarda Lima da Silva, D'Angelo Carlo Magliano, Maria Jose Campagnole-Santos, Antonio Claudio Lucas da Nóbrega, Robson Augusto Souza Santos and 1 more

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Beatriz Alexandre-SantosLaboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.
Luiza Mazzali FerrazLaboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.
Ana Beatriz ProençaLaboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.
Nícia Pedreira SoaresDepartment of Physiology and Biophysics, Institute of Biological Sciences, National Institute of Science and Technology in Nanobiopharmaceutics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Guilherme Dos Santos ReisLaboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.
Maria Eduarda Lima da SilvaLaboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.
D'Angelo Carlo MaglianoResearch Center on Morphology and Metabolism, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.
Maria Jose Campagnole-SantosDepartment of Physiology and Biophysics, Institute of Biological Sciences, National Institute of Science and Technology in Nanobiopharmaceutics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Antonio Claudio Lucas da NóbregaLaboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.
Robson Augusto Souza SantosDepartment of Physiology and Biophysics, Institute of Biological Sciences, National Institute of Science and Technology in Nanobiopharmaceutics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Eliete Dalla Corte FrantzLaboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil. elietedcf@id.uff.br.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiovascular diseases are the leading cause of death worldwide. An important mechanism involved is the disruption in protein homeostasis by overactivation of the classical axis of the renin-angiotensin system. The counterregulatory axis counteracts these effects; however, the MrgD receptor has recently been described, and its effects are unknown. Thus, this study aims to evaluate the impact of MrgD deficiency on cardiac protein homeostasis.

methods16-week-old wild-type (WT) and MrgD knockout (MrgD KO) male C57BL/6J mice were evaluated for systolic blood pressure (SBP), cardiac morphology, MDA levels, carbonyl content, and protein homeostasis markers.

resultsSBP and heart mass remained unaltered. MrgD deficiency increased left ventricular mass and led to cardiac atrophy by reduced left ventricular wall thickness and cardiomyocyte cross-sectional area. Collagen (types 1 and 3) deposition and MMP-2 cardiac protein expression were elevated in MrgD KO. Genetic deletion of MrgD increased NOX2, NOX4, and ERO1α cardiac protein expression. MDA levels were similar between groups, and carbonyl content was higher in MrgD KO. GRP78, CHOP, MuRF-1, Atrogin-1, and polyubiquitinated proteins were increased in MrgD KO mice, indicating a loss of protein homeostasis.

conclusionsThe genetic deletion of MrgD promoted cardiac remodeling and disrupted protein homeostasis, with increased pro-oxidative response and ER stress. This was associated with protein degradation by the activation of the ubiquitin-proteasome pathway.

Indexed as

MyocardiumReceptors, G-Protein-CoupledAnimalsBlood PressureEndoplasmic Reticulum Chaperone BiPGene DeletionHomeostasisMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacOxidative StressRenin-Angiotensin SystemVentricular RemodelingEndoplasmic Reticulum Chaperone BiPHspa5 protein, mouseReceptors, G-Protein-CoupledCardiac remodelingMas-related G-protein coupled receptor type D (MrgD)Protein degradationProtein homeostasisRenin-angiotensin system (RAS)

Identifiers

PMID41793552
PMCPMC12967435

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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 Socratic graph.