Mitochondria, Myocardial Remodeling, and Cardiovascular Disease

Verdejo, HE; del Campo, A; Troncoso R.; Gutiérrez T.; Toro, B; Quiroga, C; Pedrozo, Z; Munoz, JP; Garcia, L.; Castro, PF; Lavandero S.

Abstract

The process of muscle remodeling lies at the core ofmost 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. © Springer Science+Business Media, LLC 2012.

Más información

Título según WOS: Mitochondria, Myocardial Remodeling, and Cardiovascular Disease
Título según SCOPUS: Mitochondria, myocardial remodeling, and cardiovascular disease
Título de la Revista: CURRENT HYPERTENSION REPORTS
Volumen: 14
Asunto: 6
Editorial: Springer
Fecha de publicación: 2012-01-01
Página de inicio: 532
Página final: 539
Idioma: English
DOI/URL:

10.1007/s11906-012-0305-4

Identificador: 10.1007/s11906-012-0305-4
Notas: ISI, SCOPUS