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Updated: Jul 12, 2026
Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes
Published on: February 24, 2017
Evidence that human cardiac myocytes divide after myocardial infarction
A P Beltrami1, K Urbanek, J Kajstura
1Department of Medicine, New York Medical College, Valhalla 10595, USA.
Insights
The adult heart can regenerate myocytes after myocardial infarction, challenging the long-held belief that heart muscle cells do not divide. This study observed myocyte proliferation, suggesting a role in cardiac repair and increased muscle mass.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Regenerative Medicine
Background:
- Myocardial infarction (MI) traditionally implies irreversible heart damage due to non-dividing myocytes.
- Recent findings suggest adult myocytes can proliferate, questioning the postmitotic dogma.
- This study investigated myocyte division post-MI in humans.
Purpose of the Study:
- To determine the extent of myocyte mitosis in human hearts after myocardial infarction.
- To assess if adult cardiomyocytes regenerate following cardiac injury.
- To challenge the established view of the adult heart as a postmitotic organ.
Main Methods:
- Analysis of heart samples from 13 patients deceased 4-12 days post-MI, and 10 normal controls.
- Quantification of myocyte cell cycle entry using Ki-67 labeling.
- Calculation of mitotic index and observation of cell division markers (spindles, contractile rings, etc.).
Main Results:
- Ki-67 expression detected in 4% of myocytes near infarcts and 1% distant.
- Mitotic indexes of 0.08% (adjacent) and 0.03% (distant) observed.
- Evidence of mitotic spindles, contractile rings, karyokinesis, and cytokinesis confirmed myocyte proliferation.
Conclusions:
- The adult heart is not a postmitotic organ; myocytes can divide after myocardial infarction.
- Myocyte regeneration is a potential mechanism for increasing myocardial muscle mass post-MI.
- These findings have implications for understanding cardiac repair and developing regenerative therapies.
Background:
The scarring of the heart that results from myocardial infarction has been interpreted as evidence that the heart is composed of myocytes that are unable to divide. However, recent observations have provided evidence of proliferation of myocytes in the adult heart. Therefore, we studied the extent of mitosis among myocytes after myocardial infarction in humans.
Methods:
Samples from the border of the infarct and from areas of the myocardium distant from the infarct were obtained from 13 patients who had died 4 to 12 days after infarction. Ten normal hearts were used as controls. Myocytes that had entered the cell cycle in preparation for cell division were measured by labeling of the nuclear antigen Ki-67, which is associated with cell division. The fraction of myocyte nuclei that were undergoing mitosis was determined, and the mitotic index (the ratio of the number of nuclei undergoing mitosis to the number not undergoing mitosis) was calculated. The presence of mitotic spindles, contractile rings, karyokinesis, and cytokinesis was also recorded.
Results:
In the infarcted hearts, Ki-67 expression was detected in 4 percent of myocyte nuclei in the regions adjacent to the infarcts and in 1 percent of those in regions distant from the infarcts. The reentry of myocytes into the cell cycle resulted in mitotic indexes of 0.08 percent and 0.03 percent, respectively, in the zones adjacent to and distant from the infarcts. Events characteristic of cell division--the formation of the mitotic spindles, the formation of contractile rings, karyokinesis, and cytokinesis--were identified; these features demonstrated that there was myocyte proliferation after myocardial infarction.
Conclusions:
Our results challenge the dogma that the adult heart is a postmitotic organ and indicate that the regeneration of myocytes may be a critical component of the increase in muscle mass of the myocardium.
