title: Myocardial plasticity: cardiac development, regeneration and disease.
abstract: The adult mammalian heart is unable to recover from myocardial cell loss due to cardiac ischemia and infarction because terminally differentiated cardiomyocytes proliferate at a low rate. However, cardiomyocytes in other vertebrate animal models such as zebrafish, axolotls, newts and mammalian mouse neonates are capable of de-differentiating in order to promote cardiomyocyte proliferation and subsequent cardiac regeneration after injury. Although de-differentiation may occur in adult mammalian cardiomyocytes, it is typically associated with diseased hearts and pathologic remodeling rather than repair and regeneration. Here, we review recent studies of cardiac development, regeneration and disease that highlight how changes in myocardial identity (plasticity) is regulated and impacts adaptive and maladaptive cardiac responses.
authors: Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, CA 92093, USA.
authors: Joshua
authors: J
authors: Bloomekatz
authors: Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, CA 92093, USA.
authors: Manuel
authors: M
authors: Galvez-Santisteban
authors: Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, CA 92093, USA; Institute of Genomic Medicine, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: nchi@ucsd.edu.
authors: Neil C
authors: NC
authors: Chi
mesh_terms: D000558:Ambystoma mexicanum / Q000235:genetics / Q000254:growth & development; D000818:Animals; D054337:Cell Dedifferentiation / Q000235:genetics*; D049109:Cell Proliferation / Q000235:genetics; D006321:Heart / Q000254:growth & development*; D006801:Humans; D032383:Myocytes, Cardiac / Q000502:physiology*; D012038:Regeneration / Q000235:genetics*; D015027:Zebrafish / Q000235:genetics / Q000254:growth & development