PUBLICATION

Zebrafish cardiac injury and regeneration models: a noninvasive and invasive in vivo model of cardiac regeneration

Authors
Dickover, M.S., Zhang, R., Han, P., and Chi, N.C.
ID
ZDB-PUB-130923-8
Date
2013
Source
Methods in molecular biology (Clifton, N.J.)   1037: 463-473 (Chapter)
Registered Authors
Chi, Neil C., Dickover, Michael, Han, Peidong, Zhang, Ruilin
Keywords
Heart regeneration, zebrafish, resection, genetic ablation, ischemia, nitroreductase
MeSH Terms
  • Animals
  • Disease Models, Animal
  • Heart Injuries/etiology*
  • Regeneration*
  • Zebrafish*
PubMed
24029953 Full text @ Meth. Mol. Biol.
Abstract

Despite current treatment regimens, heart failure still remains one of the leading causes of morbidity and mortality in the world due to failure to adequately replace lost ventricular myocardium from ischemia-induced infarct. Although adult mammalian ventricular cardiomyocytes have a limited capacity to divide, this proliferation is insufficient to overcome the significant loss of myocardium from ventricular injury. However, lower vertebrates, such as the zebrafish and newt, have the remarkable capacity to fully regenerate their hearts after severe injury. Thus, there is great interest in studying these animal model systems to discover new regenerative approaches that might be applied to injured mammalian hearts. To this end, the zebrafish has been utilized more recently to gain additional mechanistic insight into cardiac regeneration because of its genetic tractability. Here, we describe two cardiac injury methods, a mechanical and a genetic injury model, for studying cardiac regeneration in the zebrafish.

Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping