Mitochondria, Myocardial Remodeling, and Cardiovascular Disease

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dc.contributor.authorVerdejo, Hugo E.
dc.contributor.authordel Campo, Andrea
dc.contributor.authorTroncoso, Rodrigo
dc.contributor.authorGutierrez, Tomas
dc.contributor.authorToro, Barbra
dc.contributor.authorQuiroga, Clara
dc.contributor.authorPedrozo, Zully
dc.contributor.authorPablo Munoz, Juan
dc.contributor.authorGarcia, Lorena
dc.contributor.authorCastro, Pablo F.
dc.contributor.authorLavandero, Sergio
dc.date.accessioned2025-01-24T00:06:54Z
dc.date.available2025-01-24T00:06:54Z
dc.date.issued2012
dc.description.abstractThe 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.
dc.fuente.origenWOS
dc.identifier.doi10.1007/s11906-012-0305-4
dc.identifier.eissn1534-3111
dc.identifier.issn1522-6417
dc.identifier.urihttps://doi.org/10.1007/s11906-012-0305-4
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101879
dc.identifier.wosidWOS:000310741900008
dc.issue.numero6
dc.language.isoen
dc.pagina.final539
dc.pagina.inicio532
dc.revistaCurrent hypertension reports
dc.rightsacceso restringido
dc.subjectHypertension
dc.subjectMitochondria
dc.subjectCardiomyocyte
dc.subjectOxidative stress
dc.subjectMitochondrial dynamics
dc.subjectBioenergetics
dc.subjectCardiovascular disease
dc.subjectCardiac remodeling
dc.subjectCardiac hypertrophy
dc.subjectCalcium
dc.subjectMitochondrial morphology
dc.subjectMitochondrial biogenesis
dc.subjectHeart failure
dc.subjectMitochondrial fusion
dc.subjectMitochondrial fission
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleMitochondria, Myocardial Remodeling, and Cardiovascular Disease
dc.typeartículo
dc.volumen14
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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