title: Myocyte growth and cardiac repair.
abstract: Introduced several decades ago, the dogma persists that ventricular myocytes are terminally differentiated cells and cardiac repair by myocyte regeneration is completely inhibited shortly after birth. On the basis that cardiac myocytes are unable to divide in the adult heart, myocyte growth under physiologic and pathologic conditions is believed to be restricted to cellular hypertrophy. Evidence is presented to indicate that this old paradigm has to be changed to include myocyte replication as a significant component of the cellular processes of ventricular remodeling. Importantly, myocyte death, apoptotic and necrotic in nature, has to be regarded as an additional critical variable of the multifactorial events implicated in the alterations of cardiac anatomy and myocardial structure of the decompensated heart. Methodologies are currently available to recognize and measure quantitatively the contribution of myocyte size, number and death to the adaptation of the overloaded heart and its progression to cardiac failure.
authors.affiliation: Cardiovascular Research Institute, Department of Medicine, Valhalla, New York 10595, USA. piero_anversa@nymc.edu
authors.forename: Piero
authors.initials: P
authors.lastname: Anversa
authors.forename: Annarosa
authors.initials: A
authors.lastname: Leri
authors.forename: Jan
authors.initials: J
authors.lastname: Kajstura
authors.forename: Bernardo
authors.initials: B
authors.lastname: Nadal-Ginard
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D002455:Cell Division; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D009206:Myocardium / Q000473:pathology*; D012038:Regeneration; D013234:Stem Cells / Q000166:cytology / Q000502:physiology*; D016276:Ventricular Function; D020257:Ventricular Remodeling