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논문 기본 정보

자료유형
학술저널
저자정보
Seonhwa Lee (Keimyung University Dongsan Hospital) Dong-Gi Jang (Institute for Basic Science) Yeon Ju Kyoung (Institute for Basic Science) Jeesoo Kim (Institute for Basic Science) Eui-Soon Kim (Korea Advanced Institute of Science and Technology) Ilseon Hwang (Keimyung University Dongsan Hospital) Jong-Chan Youn (Seoul St. Mary’s Hospital) Jong-Seo Kim (Institute for Basic Science) In-Cheol Kim (Keimyung University Dongsan Hospital)
저널정보
대한심장학회 Korean Circulation Journal Korean Circulation Journal Vol.54 No.8
발행연도
2024.8
수록면
468 - 481 (14page)
DOI
https://doi.org/10.4070/kcj.2024.0033

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Background and Objectives: Although 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. Methods: Comparative 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. Results: The 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. Conclusions: Different 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.

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