Related Experiment Video
Updated: Aug 22, 2026
Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes
Published on: August 28, 2016
[Is adult cardiac myocyte still able to proliferate?]
1Inserm U.572, Hôpital Lariboisière, 41, boulevard de la Chapelle, 75475 Paris Cedex 10, France. Bernard.Swynghdauw@larib.inserm.fr
Insights
Adult heart cells do not divide, leading to heart failure. Injecting progenitor cells, like bone marrow or skeletal muscle cells, can improve heart function after injury, showing promise for cardiac repair.
Area of Science:
- Cardiology
- Regenerative Medicine
- Cell Biology
Context:
- Adult cardiac myocytes lack regenerative capacity, with hypertrophy leading to heart failure.
- Non-muscular myocardial cells, including vascular endothelium, exhibit proliferation.
- Recent research suggests progenitor cells from bone marrow or endothelium contribute to myocardial adaptation.
Purpose:
- To explore the potential of progenitor cell transplantation for cardiac repair.
- To investigate methods for mimicking adaptive cardiac processes through cell injection.
- To evaluate the safety and efficacy of progenitor cell therapy in myocardial infarction.
Summary:
- Adult cardiac myocytes do not divide, and mechanically overloaded hearts typically fail after hypertrophy.
- Non-muscular cells, such as endothelial cells, can proliferate and may originate from progenitor cells.
- Injecting progenitor cells (bone marrow cells, myoblasts) into the myocardium or coronary circulation can mimic adaptive processes.
- Initial clinical trials following myocardial infarction demonstrate the safety of this approach and potential for improved cardiac function.
Impact:
- Establishes progenitor cell therapy as a potential strategy for treating heart failure and myocardial infarction.
- Highlights the regenerative potential of non-myocyte cell populations within the heart.
- Provides evidence for the safety and functional benefits of cell-based cardiac repair.
Abstract:
Adult cardiac myocytes do not divide anymore. Mechanically overloaded hearts undergo hypertrophy and then fail. Cardiac hypertrophy is mainly caused by myocyte hypertrophy without myocyte proliferation, except during end-stage heart failure. By contrast, non muscular myocardial cells, such as the endothelial cells of the vessels, not only hypertrophy but are also able to proliferate. Recent works have suggested that these new cells are likely to be progenitor cells originating from bone marrow or vascular endothelium. These cells may form chimeras in the donor heart following heart transplantation. It is possible to mimic such an adaptative process by injecting progenitor cells either within the myocardium, or through the coronary circulation. Two type of cells have been utilised so far, namely bone marrow cells and myoblasts (or satellite cells) from skeletal muscles. The first clinical applications after myocardial infarction have been recently reported and showed the safety of the procedure and the possibility of improving myocardial function.
