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Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart
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New Myocyte Formation in the Adult Heart: Endogenous Sources and Therapeutic Implications

Ronald J Vagnozzi1, Jeffery D Molkentin2,3, Steven R Houser4

  • 1From the Department of Pediatrics (R.J.V., J.D.M.).

Circulation Research
|July 7, 2018
PubMed

Insights

Adult heart cells (cardiac myocytes) cannot regenerate after injury. New research suggests focusing on existing myocyte proliferation, not progenitor cells, for heart repair therapies.

Area of Science:

  • Cardiovascular Biology
  • Regenerative Medicine
  • Cardiac Pathophysiology

Background:

  • Cardiovascular diseases lead to adult cardiac myocyte death, driving pathological ventricular remodeling and heart failure.
  • Current therapies, excluding heart transplantation, cannot replace lost cardiac myocytes.
  • Limited understanding of endogenous myocyte turnover hinders regenerative strategies for injured hearts.

Purpose of the Study:

  • To investigate the cellular sources and intrinsic capacity for endogenous cardiac myocyte turnover in adult mammals.
  • To inform the development of innovative therapeutic strategies for cardiac regeneration after injury.

Main Methods:

  • Review of existing literature on cardiac myocyte proliferation and progenitor cell activity.
  • Analysis of the consensus regarding endogenous mechanisms of myocyte renewal.

Main Results:

  • A growing consensus indicates that the limited capacity for new myocyte formation in adult hearts stems from the proliferation of existing cardiac myocytes.
  • Evidence does not support the activity of an endogenous progenitor cell source for myocyte regeneration.

Conclusions:

  • Future therapeutic approaches for cardiac regeneration must consider the fundamental biology of myocyte renewal, focusing on existing myocyte proliferation.
  • Strategies to replenish lost myocytes in injured hearts should be designed based on this understanding of myocyte turnover.

Keywords:
cell proliferationheart failuremyocardial infarctionregenerationstem cell

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