Key result
Myocardial infarction is linked to ~12-fold higher cardiomyocyte mitosis and cytokinesis in adult human hearts.
Why the study?
Rodent MI models show increased cardiomyocyte mitosis in response to ischemia, but this has not been shown in humans.
Observational
No
This study provides the first evidence that adult human cardiomyocytes possess an intrinsic capacity to increase mitosis and cytokinesis in response to myocardial infarction, highlighting a potential therapeutic target for cardiac regeneration.
Supports potential intrinsic regeneration in adult human hearts; leaves open therapeutic translation pending prospective validation.
BACKGROUND: Myocardial infarction (MI) is a leading cause of death worldwide and can eliminate up to a third of the cardiomyocytes within the human heart. Although cardiomyocytes undergo mitosis during early development, most cardiomyocytes cease cell cycling soon after birth. In contrast, rodent MI models have shown that cardiomyocytes increase mitosis in response to ischemia; however, this has not been shown in humans. METHODS: Using a unique premortem post-MI human heart, immunostaining, bulk RNA sequencing, proteomics, metabolomics, single-nucleus RNA sequencing and a novel post-MI human biopsy method, we investigated human cardiomyocyte mitosis post-MI. RESULTS: We show that adult human cardiomyocytes exhibit increased mitosis and cytokinesis in response to ischemia. CONCLUSIONS: Future development of therapeutics to enhance this intrinsic mitotic potential could lead to new treatments that reverse heart failure via cardiac regeneration.
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Hume et al. (2025) conducted an observational in Myocardial Infarction. Ischemia from myocardial infarction vs. Non-ischemic donor left ventricle or remote non-ischemic myocardium was evaluated on Cardiomyocyte mitosis and cytokinesis (proportion of pH3+ and MKLP1+ cardiomyocytes). Myocardial infarction stimulated an intrinsic increase in cardiomyocyte mitosis and cytokinesis in the ischemic adult human heart compared to non-ischemic controls.
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