Lookup NU author(s): Dr Langping He,
Dr Matt Bates,
Professor Robert Taylor
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
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.
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
Print publication date: 01/03/2016
Online publication date: 30/09/2015
Acceptance date: 25/09/2015
Date deposited: 31/03/2016
ISSN (print): 1054-8807
ISSN (electronic): 1879-1336
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