Cell-cycle-based strategies to drive myocardial repair
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Updated: Jun 24, 2026
Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
Wuqiang Zhu1, Rutger J Hassink, Michael Rubart
1The Riley Heart Research Center, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, 1044 West Walnut Street, R4 Building Room W376, Indianapolis, IN 46202-5225, USA.
Insights
Postnatal heart regeneration is limited. Inducing cardiomyocyte cell cycle proliferation with cyclin D2 in mice improved cardiac repair and function after injury, suggesting cell-cycle strategies for myocardial repair.
Area of Science:
- Cardiovascular biology
- Regenerative medicine
- Molecular cardiology
Background:
- Cardiomyocytes (heart muscle cells) proliferate actively during development but lose this capacity after birth.
- Limited cardiomyocyte proliferation in the postnatal heart restricts natural repair following cardiac injury.
Purpose of the Study:
- To review studies investigating the induction of cardiomyocyte cell cycle proliferation in postnatal hearts.
- To evaluate the potential of cell-cycle-based strategies for myocardial repair.
Main Methods:
- Targeted expression of cyclin D2 in postnatal hearts of transgenic mice.
- Assessment of cardiomyocyte cell cycle activity compared to non-transgenic controls.
- Evaluation of cardiac function and infarct size after induced injury (coronary artery occlusion).
Main Results:
- Cyclin D2 expression led to over a 500-fold increase in cardiomyocyte cell cycle activity.
- Induced proliferation resulted in significant infarct regression.
- Improved cardiac hemodynamics were observed following coronary artery occlusion in treated mice.
Conclusions:
- Targeted induction of cardiomyocyte cell cycle proliferation is feasible in postnatal hearts.
- Cell-cycle-based strategies show promise for driving myocardial repair and improving cardiac function after injury.
Abstract:
Cardiomyocytes exhibit robust proliferative activity during development. After birth, cardiomyocyte proliferation is markedly reduced. Consequently, regenerative growth in the postnatal heart via cardiomyocyte proliferation (and, by inference, proliferation of stem-cell-derived cardiomyocytes) is limited and often insufficient to affect repair following injury. Here, we review studies wherein cardiomyocyte cell cycle proliferation was induced via targeted expression of cyclin D2 in postnatal hearts. Cyclin D2 expression resulted in a greater than 500-fold increase in cell cycle activity in transgenic mice as compared to their nontransgenic siblings. Induced cell cycle activity resulted in infarct regression and concomitant improvement in cardiac hemodynamics following coronary artery occlusion. These studies support the notion that cell-cycle-based strategies can be exploited to drive myocardial repair following injury.
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