Mitochondria, myocardial remodeling, and cardiovascular disease
MetadataShow full item record
The process of muscle remodeling lies at the core of most cardiovascular diseases. Cardiac adaptation to pressure or volume overload is associated with a complex molecular change in cardiomyocytes which leads to anatomic remodeling of the heart muscle. Although adaptive at its beginnings, the sustained cardiac hypertrophic remodeling almost unavoidably ends in progressive muscle dysfunction, heart failure and ultimately death. One of the features of cardiac remodeling is a progressive impairment in mitochondrial function. The heart has the highest oxygen uptake in the human body and accordingly it has a large number of mitochondria, which form a complex network under constant remodeling in order to sustain the high metabolic rate of cardiac cells and serve as Ca2+ buffers acting together with the endoplasmic reticulum (ER). However, this high dependence on mitochondrial metabolism has its costs: when oxygen supply is threatened, high leak of electrons from the electron transport chain leads to oxidative stress and mitochondrial failure. These three aspects of mitochondrial function (Reactive oxygen species signaling, Ca2+ handling and mitochondrial dynamics) are critical for normal muscle homeostasis. In this article, we will review the latest evidence linking mitochondrial morphology and function with the process of myocardial remodeling and cardiovascular disease.
Artículo de publicación SCOPUS
Quote ItemCurrent Hypertension Reports, Volumen 14, Issue 6, 2012, Pages 532-539
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile
Showing items related by title, author, creator and subject.
Corrigendum to “The novel mitochondrial iron chelator 5-((methylamino)methyl)-8-hydroxyquinoline protects against mitochondrial-induced oxidative damage and neuronal death” [Biochem. Biophys. Res. Commun. 463 (4) (2015) 787-792] Mena, Natalia P.; García Beltrán, Olimpo; Lourido, Fernanda; Urrutia, Pamela J.; Mena, Raúl; Castro Castillo, Vicente; Cassels Niven, Bruce; Núñez González, Marco (Elsevier, 2016)
Mitochondrial permeability transition pore contributes to mitochondrial dysfunction in fibroblasts of patients with sporadic Alzheimer's disease Pérez, María José; Ponce, Daniela P.; Aranguiz, Alejandra; Behrens Pellegrino, María Isabel; Quintanilla, Rodrigo A. (Elsevier B.V., 2018)© 2018 The Authors In the last few decades, many reports have suggested that mitochondrial function impairment is a hallmark of Alzheimer's disease (AD). Although AD is a neurodegenerative disorder, mitochondrial damage ...
The novel mitochondrial iron chelator 5-((methylamino)methyl)-8-hydroxyquinoline protects against mitochondrial-induced oxidative damage and neuronal death Mena, Natalia P.; García Beltrán, Olimpo; Lourido, Fernanda; Urrutia, Pamela J.; Mena, Raúl; Castro Castillo, Vicente; Cassels Niven, Bruce; Núñez González, Marco (Elsevier, 2015)Abundant evidence indicates that iron accumulation, oxidative damage and mitochondrial dysfunction are common features of Huntington's disease, Parkinson's disease, Friedreich's ataxia and a group of disorders known as ...