Evidence map›Paper›PMID 34292883›Full record

ArticleJCI insight2021

MG53 suppresses NF-κB activation to mitigate age-related heart failure.

Xiaoliang Wang, Xiuchun Li, Hannah Ong, Tao Tan, Ki Ho Park, Zehua Bian, Xunchang Zou, Erin Haggard, Paul M Janssen, Robert E Merritt and 7 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  11. Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025
    Review
  12. Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025
    Review
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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

17 authors at 2 institutions in 1 country.

Xiaoliang WangDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Xiuchun LiDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Hannah OngDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Tao TanDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Ki Ho ParkDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Zehua BianDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Xunchang ZouDepartment of Cancer Biology and Genetics, College of Medicine, and.
Erin HaggardDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Paul M JanssenDepartment of Physiology and Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Robert E MerrittDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Timothy M PawlikDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Bryan A WhitsonDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Nahush A MokadamDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Lei CaoDepartment of Cancer Biology and Genetics, College of Medicine, and.
Hua ZhuDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Chuanxi CaiDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Jianjie MaDepartment of Surgery, Division of Cardiac Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Lung Institute · USThe Ohio State University · US

Funding

MG53-Mediated Membrane Repair in Muscle Physiology and DiseaseR01AR061385 · NIAMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI LIN, PEI-HUI · 2011 to 2020
$3.8M
Cancer Prevention and Treatment by Activation of a Brain-Adipocyte AxisR01CA166590 · NCI · OHIO STATE UNIVERSITY · PI CAO, LEI · 2013 to 2022
$3.4M
Protein therapeutic to facilitate healing of chronic wounds.R44GM123887 · NIGMS · TRIM-EDICINE, INC. · PI TAN, TAO · 2019 to 2021
$1.8M
Myokine function of MG53 in muscle injury-repair and regenerationR01AR070752 · NIAMS · OHIO STATE UNIVERSITY · PI HAN, RENZHI · 2017 to 2021
$1.7M
Inhibiting Cell Death for Protecting Cardiac InjuryR01HL153876 · NHLBI · OHIO STATE UNIVERSITY · PI ZHU, HUA · 2020 to 2023
$1.6M
Protein therapeutic to facilitate healing of chronic wounds.R43GM123887 · NIGMS · TRIM-EDICINE, INC. · PI TAN, TAO · 2017 to 2017
$262k
NCI NIH HHS R01 CA166590NHLBI NIH HHS R01 HL153876NIAMS NIH HHS R01 AR061385NIAMS NIH HHS R01 AR070752NIGMS NIH HHS R43 GM123887NIGMS NIH HHS R44 GM123887
6 · The paper itself

Abstract

Aging is associated with chronic oxidative stress and inflammation that affect tissue repair and regeneration capacity. MG53 is a TRIM family protein that facilitates repair of cell membrane injury in a redox-dependent manner. Here, we demonstrate that the expression of MG53 was reduced in failing human hearts and aged mouse hearts, concomitant with elevated NF-κB activation. We evaluated the safety and efficacy of longitudinal, systemic administration of recombinant human MG53 (rhMG53) protein in aged mice. Echocardiography and pressure-volume loop measurements revealed beneficial effects of rhMG53 treatment in improving heart function of aged mice. Biochemical and histological studies demonstrated that the cardioprotective effects of rhMG53 are linked to suppression of NF-κB-mediated inflammation, reducing apoptotic cell death and oxidative stress in the aged heart. Repetitive administration of rhMG53 in aged mice did not have adverse effects on major vital organ functions. These findings support the therapeutic value of rhMG53 in treating age-related decline in cardiac function.

Indexed as

AgingGene Expression RegulationOxidative StressAgedAnimalsApoptosisDisease Models, AnimalEchocardiographyFemaleHeart FailureHumansMaleMembrane ProteinsMiceMice, Inbred C57BLMiddle AgedMembrane ProteinsMG53 protein, mouseNF-kappa BRNAAgingCardiologyHeart failureMouse modelsNF-kappaB

Identifiers

PMID34292883
PMCPMC8492351
OpenAlexW3186505531

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.