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Impaired mitochondrial biogenesis is a common feature to myocardial hypertrophy and end-stage ischemic heart failure

Lookup NU author(s): Dr Langping He, Dr Matt Bates, Professor Robert Taylor

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

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.


Publication metadata

Author(s): Pisano A, Cerbelli B, Perli E, Pelullo M, Bargelli V, Preziuso C, Mancini M, He LP, Bates MGD, Lucena JR, Della Monica PL, Familiari G, Petrozza V, Nediani C, Taylor RW, d'Amati G, Giordano C

Publication type: Article

Publication status: Published

Journal: Cardiovascular Pathology

Year: 2016

Volume: 25

Issue: 2

Pages: 103-112

Print publication date: 01/03/2016

Online publication date: 30/09/2015

Acceptance date: 25/09/2015

ISSN (print): 1054-8807

ISSN (electronic): 1879-1336

Publisher: Elsevier

URL: http://dx.doi.org/10.1016/j.carpath.2015.09.009

DOI: 10.1016/j.carpath.2015.09.009


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