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Updated: Mar 14, 2026

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes
Published on: February 24, 2017
Understanding cardiomyocyte proliferation: an insight into cell cycle activity
Murugavel Ponnusamy1, Pei-Feng Li2, Kun Wang3
1Center for Developmental Cardiology, Institute of Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266021, China.
Insights
Adult cardiomyocytes can divide, challenging old beliefs. Understanding cardiomyocyte cell cycle regulation is crucial for developing therapies for heart repair and regeneration.
Area of Science:
- Cardiovascular Biology
- Cell Cycle Regulation
- Regenerative Medicine
Background:
- Myocardial injury recovery relies on cardiomyocyte proliferation and regeneration.
- Recent research indicates adult cardiomyocytes can re-enter the cell cycle, contrary to prior assumptions.
- Targeting cardiomyocyte cell cycle activity presents a promising therapeutic avenue for cardiac repair.
Purpose of the Study:
- To review recent advancements in understanding cardiomyocyte cell cycle activity across different life stages (gestation, birth, adulthood).
- To detail the expression and activity of key cell cycle regulators (cyclins, CDKs, inhibitors, associated proteins) during cardiac development.
- To explore the influence of transcription factors, microRNAs, and signaling pathways (PI3K/AKT, Wnt/β-catenin, Hippo-YAP) on cardiomyocyte cell cycle progression.
Main Methods:
- Literature review of studies on cardiomyocyte cell cycle.
- Analysis of temporal expression patterns of cell cycle proteins.
- Examination of signaling pathways and regulatory molecules influencing cell cycle activity.
Main Results:
- Cardiomyocyte cell cycle activity differs significantly between neonatal and adult stages.
- Specific cyclins, CDKs, inhibitors (p21, p27, p57, p16, p18), and proteins (Rb, p107, p130) show dynamic temporal expression.
- Transcription factors, microRNAs, and pathways like PI3K/AKT, Wnt/β-catenin, and Hippo-YAP modulate cardiomyocyte cell cycle progression.
- Postnatal structural and cellular changes contribute to the cessation of cardiomyocyte cell cycle activity.
Conclusions:
- The review highlights the plasticity of cardiomyocyte cell cycle regulation throughout life.
- Understanding these mechanisms is vital for developing effective cardiac regeneration strategies.
- Targeting specific pathways and molecules could restore proliferative capacity in adult cardiomyocytes for therapeutic benefit.
Abstract:
Cardiomyocyte proliferation and regeneration are key to the functional recovery of myocardial tissue from injury. In the recent years, studies on cardiomyocyte proliferation overturned the traditional belief that adult cardiomyocytes permanently withdraw from the cell cycle activity. Hence, targeting cardiomyocyte proliferation is one of the potential therapeutic strategies for myocardial regeneration and repair. To achieve this, a deep understanding of the fundamental mechanisms involved in cardiomyocyte cell cycle as well as differences between neonatal and adult cardiomyocytes' cell cycle activity is required. This review focuses on the recent progress in understanding of cardiomyocyte cell cycle activity at different life stages viz., gestation, birth, and adulthood. The temporal expression/activities of major cell cycle activators (cyclins and CDKs), inhibitors (p21, p27, p57, p16, and p18), and cell-cycle-associated proteins (Rb, p107, and p130) in cardiomyocytes during gestation and postnatal life are described in this review. The influence of different transcription factors and microRNAs on the expression of cell cycle proteins is demonstrated. This review also deals major pathways (PI3K/AKT, Wnt/β-catenin, and Hippo-YAP) associated with cardiomyocyte cell cycle progression. Furthermore, the postnatal alterations in structure and cellular events responsible for the loss of cell cycle activity are also illustrated.
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