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Updated: Oct 25, 2025
Simultaneous Assessment of Cardiomyocyte DNA Synthesis and Ploidy: A Method to Assist Quantification of Cardiomyocyte Regeneration and Turnover
Published on: May 23, 2016
Cardiomyocyte Proliferation as a Source of New Myocyte Development in the Adult Heart
Jaslyn Johnson1, Sadia Mohsin1, Steven R Houser1
1Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Insights
Regenerating heart muscle after myocardial infarction (MI) is crucial for treating heart failure (HF). This review explores methods to induce cardiomyocyte division for cardiac repair while avoiding risks like cancer.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Cell Biology
Background:
- Myocardial infarction (MI) causes cardiomyocyte death, leading to heart failure (HF) and impaired cardiac function.
- Current therapies offer limited cardiac regeneration, highlighting the need for strategies to replace lost myocardium.
- Inducing new myocyte formation from existing cardiomyocytes is a promising therapeutic avenue.
Purpose of the Study:
- To review studies inducing cardiomyocyte cell cycle re-entry after cardiac injury.
- To assess whether cardiomyocytes complete cytokinesis (cell division) in response to interventions.
- To address limitations and methodological advancements in identifying new myocyte formation.
Main Methods:
- Review of existing literature on cardiomyocyte cell cycle manipulation.
- Analysis of studies focusing on signaling pathways, gene expression, and environmental factors.
- Evaluation of methods for distinguishing cardiomyocyte division from DNA synthesis.
Main Results:
- Terminally differentiated myocytes can be prompted to re-enter the cell cycle.
- Approaches vary in efficacy, with some leading to minimal myocyte renewal or pathological cardiomegaly.
- Accurate identification of cardiomyocyte division versus DNA synthesis remains a challenge.
Conclusions:
- Optimizing cardiomyocyte proliferation for myocardial regeneration without inducing tumorigenesis is a significant challenge.
- Further methodological advancements are needed to reliably confirm new myocyte formation.
- Successful cardiac regeneration strategies require precise control over cardiomyocyte cell cycle activity.
Abstract:
Cardiac diseases such as myocardial infarction (MI) can lead to adverse remodeling and impaired contractility of the heart due to widespread cardiomyocyte death in the damaged area. Current therapies focus on improving heart contractility and minimizing fibrosis with modest cardiac regeneration, but MI patients can still progress to heart failure (HF). There is a dire need for clinical therapies that can replace the lost myocardium, specifically by the induction of new myocyte formation from pre-existing cardiomyocytes. Many studies have shown terminally differentiated myocytes can re-enter the cell cycle and divide through manipulations of the cardiomyocyte cell cycle, signaling pathways, endogenous genes, and environmental factors. However, these approaches result in minimal myocyte renewal or cardiomegaly due to hyperactivation of cardiomyocyte proliferation. Finding the optimal treatment that will replenish cardiomyocyte numbers without causing tumorigenesis is a major challenge in the field. Another controversy is the inability to clearly define cardiomyocyte division versus myocyte DNA synthesis due to limited methods. In this review, we discuss several studies that induced cardiomyocyte cell cycle re-entry after cardiac injury, highlight whether cardiomyocytes completed cytokinesis, and address both limitations and methodological advances made to identify new myocyte formation.
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