Evidence map›Paper›PMID 38956938›Full record

ArticleKorean circulation journal2024

Proteome-wide Characterization and Pathophysiology Correlation in Non-ischemic Cardiomyopathies.

Seonhwa Lee, Dong-Gi Jang, Yeon Ju Kyoung, Jeesoo Kim, Eui-Soon Kim, Ilseon Hwang, Jong-Chan Youn, Jong-Seo Kim, In-Cheol Kim

Abstract read
In one paragraph

Article in Korean circulation journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Seonhwa Lee *Division of Cardiology, Department of Internal Medicine, Cardiovascular Center, Keimyung University Dongsan Hospital, Keimyung University School of Medicine, Daegu, Korea.ORCID https://orcid.org/0000-0002-1620-795X
Dong-Gi Jang *Center for RNA Research, Institute for Basic Science, Seoul, Korea.ORCID https://orcid.org/0009-0005-0861-188X
Yeon Ju KyoungCenter for RNA Research, Institute for Basic Science, Seoul, Korea.ORCID https://orcid.org/0009-0007-3607-5361
Jeesoo KimCenter for RNA Research, Institute for Basic Science, Seoul, Korea.ORCID https://orcid.org/0009-0006-0528-8308
Eui-Soon KimGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Korea.ORCID https://orcid.org/0000-0003-2313-8646
Ilseon HwangDepartment of Pathology, Keimyung University Dongsan Hospital, Keimyung University School of Medicine, Daegu, Korea.ORCID https://orcid.org/0000-0002-6122-4417
Jong-Chan YounDivision of Cardiology, Department of Internal Medicine, Seoul St. Mary's Hospital, Catholic Research Institute for Intractable Cardiovascular Disease, College of Medicine, The Catholic University of Korea, Seoul, Korea. jong.chan.youn@gmail.com.ORCID https://orcid.org/0000-0003-0998-503X
Jong-Seo KimCenter for RNA Research, Institute for Basic Science, Seoul, Korea.ORCID https://orcid.org/0000-0002-8909-8440
In-Cheol KimDivision of Cardiology, Department of Internal Medicine, Cardiovascular Center, Keimyung University Dongsan Hospital, Keimyung University School of Medicine, Daegu, Korea. kimic@dsmc.or.kr.ORCID https://orcid.org/0000-0002-5751-2328

Funding

Korea Health Industry Development Institute HI22C0198Korean Cardiac Research Foundation 202202-01Ministry of Science and ICT, South Korea IBS-R008-D1National Research Foundation of Korea NRF-2020R1C1C1014161National Research Foundation of Korea NRF-2021R1A5A1033157National Research Foundation of Korea NRF-2021R1F1A1063430Seoul St. Mary's Hospital, Catholic University of Korea
6 · The paper itself

Abstract

BACKGROUND AND

objectivesAlthough the clinical consequences of advanced heart failure (HF) may be similar across different etiologies of cardiomyopathies, their proteomic expression may show substantial differences in relation to underlying pathophysiology. We aimed to identify myocardial tissue-based proteomic characteristics and the underlying molecular pathophysiology in non-ischemic cardiomyopathy with different etiologies.

methodsComparative extensive proteomic analysis of the myocardium was performed in nine patients with biopsy-proven non-ischemic cardiomyopathies (3 dilated cardiomyopathy [DCM], 2 hypertrophic cardiomyopathy [HCM], and 4 myocarditis) as well as five controls using tandem mass tags combined with liquid chromatography-mass spectrometry. Differential protein expression analysis, Gene Ontology (GO) analysis, and Ingenuity Pathway Analysis (IPA) were performed to identify proteomic differences and molecular mechanisms in each cardiomyopathy type compared to the control. Proteomic characteristics were further evaluated in accordance with clinical and pathological findings.

resultsThe principal component analysis score plot showed that the controls, DCM, and HCM clustered well. However, myocarditis samples exhibited scattered distribution. IPA revealed the downregulation of oxidative phosphorylation and upregulation of the sirtuin signaling pathway in both DCM and HCM. Various inflammatory pathways were upregulated in myocarditis with the downregulation of Rho GDP dissociation inhibitors. The molecular pathophysiology identified by extensive proteomic analysis represented the clinical and pathological properties of each cardiomyopathy with abundant proteomes.

conclusionsDifferent etiologies of non-ischemic cardiomyopathies in advanced HF exhibit distinct proteomic expression despite shared pathologic findings. The benefit of tailored management strategies considering the different proteomic expressions in non-ischemic advanced HF requires further investigation.

Indexed as

CardiomyopathyHeart failurePathologyProteomics

Identifiers

PMID38956938
PMCPMC11306425

What Socratic holds

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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.