期刊
CARDIOVASCULAR PATHOLOGY
卷 25, 期 2, 页码 103-112出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.carpath.2015.09.009
关键词
Cardiac remodeling; Myocardial hypertrophy; mtDNA depletion; Mitochondrial biogenesis; Oxidative stress; Mitochondrial cardiomyopathy
资金
- Wellcome Trust [096919/Z/11/Z]
- MRC Centre for Neuromuscular Diseases [G0601943]
- Lily Foundation
- UK NHS Highly Specialised Rare Mitochondrial Disorders of Adults and Children Service
- Associazione Serena Talarico per i Giovani nel Mondo
- Fondazione Giuseppe Tomasello ONLUS
- Mitocon Onlus
- MRC [MR/K000608/1, G0601943] Funding Source: UKRI
- Medical Research Council [G0601943, MR/K000608/1] Funding Source: researchfish
Mitochondrial (mt) DNA depletion and oxidative mtDNA damage have been implicated in the process of pathological cardiac remodeling. Whether these features are present in the early phase of maladaptive cardiac remodeling, that is, during compensated cardiac hypertrophy, is still unknown. We compared the morphologic and molecular features of mt biogenesis and markers of oxidative stress in human heart from adult subjects with compensated hypertrophic cardiomyopathy and heart failure. We have shown that mtDNA depletion is a constant feature of both conditions. A quantitative loss of mtDNA content was associated with significant down-regulation of selected modulators of mt biogenesis and decreased expression of proteins involved in mtDNA maintenance. Interestingly, mtDNA depletion characterized also the end-stage phase of cardiomyopathies due to a primary mtDNA defect. Oxidative stress damage was detected only in failing myocardium. (C) 2015 The Authors. Published by Elsevier Inc.
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