PUBLICATION

Myocardial plasticity: cardiac development, regeneration and disease

Authors
Bloomekatz, J., Galvez-Santisteban, M., Chi, N.C.
ID
ZDB-PUB-160809-9
Date
2016
Source
Current opinion in genetics & development   40: 120-130 (Review)
Registered Authors
Bloomekatz, Joshua, Chi, Neil C.
Keywords
none
MeSH Terms
  • Ambystoma mexicanum/genetics
  • Ambystoma mexicanum/growth & development
  • Animals
  • Cell Dedifferentiation/genetics*
  • Cell Proliferation/genetics
  • Heart/growth & development*
  • Humans
  • Myocytes, Cardiac/physiology*
  • Regeneration/genetics*
  • Zebrafish/genetics
  • Zebrafish/growth & development
PubMed
27498024 Full text @ Curr. Opin. Genet. Dev.
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.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping