Evidence map›Paper›PMID 35526242›Full record

ArticleMolecular biology reports2022

Changes in AMPKα and Ubiquitin Ligases in Myocyte Reverse Remodeling after Surgical Ventricular Reconstruction in rats with ischemic cardiomyopathy.

Yasushige Shingu, Tetsuya Hieda, Satoshi Sugimoto, Hidetsugu Asai, Tomoji Yamakawa, Satoru Wakasa

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Article in Molecular biology reports, 2022. 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

What it found

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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.

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5 · Who and what money

Authors and funding

6 authors at 5 institutions in 1 country.

Yasushige ShinguDepartment of Cardiovascular and Thoracic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan. shingu@huhp.hokudai.ac.jp.ORCID http://orcid.org/0000-0001-8471-5166
Tetsuya HiedaDepartment of Cardiovascular and Thoracic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Satoshi SugimotoDepartment of Cardiovascular Surgery, Obihiro Kosei Hospital, Obihiro, Japan.
Hidetsugu AsaiDepartment of Cardiovascular Surgery, Hokkaido Medical Center for Child Health and Rehabilitation, Sapporo, Japan.
Tomoji YamakawaDepartment of Cardiovascular Surgery, Kinikyo Chuo Hospital, Sapporo, Japan.
Satoru WakasaDepartment of Cardiovascular and Thoracic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Hokkaido University · JPHokkaido University of Science · JPKin-ikyo Chuo Hospital · JPNational Hospital Organization Hokkaido Medical Center · JPObihiro Kosei General Hospital · JP

Funding

Japan Heart Foundation Research Grant 2015 NAMochida Memorial Foundation for Medical and Pharmaceutical Research 2016 NA
6 · The paper itself

Abstract

backgroundThe change in myocardial protein degradation systems after ventricular unloading has been unknown. We aimed to evaluate the anti-hypertrophic protein adenosine monophosphate-activated protein kinase (AMPK) and two major protein degradation systems (ubiquitin proteasome system and autophagy) in a model of surgical ventricular reconstruction (SVR) in rats with ischemic cardiomyopathy. METHODS AND

resultsRats were randomized into the following groups: sham/sham (control group), myocardial infarction (MI)/sham (sham group) and MI/SVR (SVR group), with an interval of 4 weeks. Two (early, n = 5 for each) and 28 days (late, n = 5 for each) after SVR, ventricular size, and wall stress were assessed. Myocyte area, protein expression of AMPKα and autophagy markers, and gene expression of ubiquitin ligases (Atrogin-1 and Murf-1) were evaluated in the late phase. In the early phase, left ventricular dimensions and wall stress were smaller in the SVR group than in the sham group, whereas they were comparable in the late period. Myocyte area in the SVR group was reduced to the value in the control group, while it was larger in the sham group than in the control group. Total-AMPKα, p-AMPKα, and AMPKα phosphorylation rates were higher, and Atrogin-1 and Murf-1 were lower in the SVR group than in the sham group, while the autophagy markers were not different between the groups. p-AMPKα had strong negative correlations with myocyte area, Atrogin-1, and Murf-1.

conclusionsIn myocyte reverse remodeling after SVR, AMPKα phosphorylation increased in association with reduced gene expression of ubiquitin ligases.

Indexed as

CardiomyopathiesMyocardial InfarctionAMP-Activated Protein KinasesAnimalsHeart VentriclesMuscle CellsRatsUbiquitinUbiquitin-Protein LigasesVentricular RemodelingAMP-Activated Protein KinasesUbiquitinUbiquitin-Protein LigasesAMPKαAtrogin-1Murf-1Myocyte reverse remodelingSurgical ventricular reconstruction

Identifiers

PMID35526242
OpenAlexW4229332295

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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.