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

Autor: Pisano A; Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy., Cerbelli B; Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy., Perli E; Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy., Pelullo M; Department of Molecular Medicine, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy., Bargelli V; Department of Biochemical Sciences, University of Florence, Viale Morgagni, 50, 50134, Florence, Italy., Preziuso C; Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy., Mancini M; Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy; Department of Molecular Medicine, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy., He L; Wellcome Trust Centre for Mitochondrial Research, Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK., Bates MG; Wellcome Trust Centre for Mitochondrial Research, Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK., Lucena JR; Forensic Pathology Service, Institute of Legal Medicine, Seville, Spain., Della Monica PL; Department of Cardiac Surgery and Transplantation, San Camillo Hospital, Rome, Italy., Familiari G; Department of Human Anatomic, Histologic, Forensic and Locomotor Apparatus Sciences, Sapienza University, 00161, Rome, Italy., Petrozza V; Department of Biotechnologies and medical and Surgical Sciences, Sapienza University, 00161, Rome, Italy., Nediani C; Department of Biochemical Sciences, University of Florence, Viale Morgagni, 50, 50134, Florence, Italy., Taylor RW; Wellcome Trust Centre for Mitochondrial Research, Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK., d'Amati G; Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy., Giordano C; Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Policlinico Umberto I, Viale Regina Elena 324, 00161, Rome, Italy. Electronic address: carla.giordano@uniroma1.it.
Jazyk: angličtina
Zdroj: Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology [Cardiovasc Pathol] 2016 Mar-Apr; Vol. 25 (2), pp. 103-12. Date of Electronic Publication: 2015 Sep 30.
DOI: 10.1016/j.carpath.2015.09.009
Abstrakt: 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.
(Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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