Cyclin A2 induces cardiac regeneration after myocardial infarction and prevents heart failure. Academic Article uri icon

Overview

abstract

  • Mammalian myocardial infarction is typically followed by scar formation with eventual ventricular dilation and heart failure. Here we present a novel model system in which mice constitutively expressing cyclin A2 in the myocardium elicit a regenerative response after infarction and exhibit significantly limited ventricular dilation with sustained and remarkably enhanced cardiac function. New cardiomyocyte formation was noted in the infarcted zones as well as cell cycle reentry of periinfarct myocardium with an increase in DNA synthesis and mitotic indices. The enhanced cardiac function was serially assessed over time by MRI. Furthermore, the constitutive expression of cyclin A2 appears to augment endogenous regenerative mechanisms via induction of side population cells with enhanced proliferative capacity. The ability of cultured transgenic cardiomyocytes to undergo cytokinesis provides mechanistic support for the regenerative capacity of cyclin A2.

publication date

  • May 10, 2007

Research

keywords

  • Cardiac Output, Low
  • Cyclin A
  • Heart
  • Myocardial Infarction
  • Myocytes, Cardiac
  • Regeneration

Identity

Scopus Document Identifier

  • 34250857995

PubMed ID

  • 17495221

Additional Document Info

volume

  • 100

issue

  • 12