title: [Cardiac hypertrophy: molecular and cellular events].
abstract: Cardiac hypertrophy is one of the main ways in which cardiomyocytes respond to mechanical and neurohormonal stimuli. It enables myocytes to increase their work output, which improves cardiac pump function. However, this compensatory mechanism can become overwhelmed by biomechanical stress, thereby resulting in heart failure, which is associated with high morbidity and mortality. The complex molecular processes that lead to cardiomyocyte growth involve membrane receptors, second messengers, and transcription factors. The common final pathway of all these intracellular substances is gene expression, whose variations are being revealed in increasing detail. The genetic response is characterized by the re-expression of fetal genes, an event which is regarded as the molecular marker of pathologic cardiac hypertrophy, and which is absent in normal physiologic cardiac growth. The possibility of stopping or reversing pathologic cardiac hypertrophy and, thereby, slowing the development of heart failure is a topic of considerable clinical interest and a large amount of relevant data has accumulated. The purpose of this review was to provide a schematic overview of current knowledge about the molecular pathogenesis of cardiomyocyte hypertrophy, with special emphasis on new research topics and investigations.
authors.affiliation: Laboratorio de Cardiología Molecular, Departamento de Enfermedades Cardiovasculares, Escuela de Medicina, Pontificia Universidad Católica de Chile, Lira 85, piso 2, Santiago, Chile.
authors.forename: Juan Eduardo
authors.initials: JE
authors.lastname: Carreño
authors.forename: Felipe
authors.initials: F
authors.lastname: Apablaza
authors.forename: María Paz
authors.initials: MP
authors.lastname: Ocaranza
authors.forename: Jorge E
authors.initials: JE
authors.lastname: Jalil
mesh_terms: D006332:Cardiomegaly / Q000235:genetics* / Q000503:physiopathology*; D006801:Humans; D032383:Myocytes, Cardiac / Q000473:pathology / Q000502:physiology; D015398:Signal Transduction