ArticleCirculation research2026
Human Hearts Intrinsically Increase Cardiomyocyte Mitosis After Myocardial Infarction.
Article in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- NEAT1 Coordinates a PDLIM5-CACNA1C Regulatory Program Associated with a Potentially Arrhythmogenic Cardiomyocyte State in the Border Zone During Early Myocardial Infarction.International journal of molecular sciences · 2026Article
- Lamin B1 loss in human cardiomyocytes is associated with nuclear shape deformation in dilated cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Article
- Multi-Omics Integration Reveals Incomplete Reactivation of Developmental Cell-Cycle Programs in Adult Human Infarcted Hearts.Chemical biology & drug design · 2026Article
- Beyond autophagic flux: selective autophagy adaptors and cargo prioritization in cardiac disease.Cardiology plusReview
Corrections and comments
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Authors and funding
26 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial 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.
methodsUsing 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.
resultsWe show that adult human cardiomyocytes exhibit increased mitosis and cytokinesis in response to ischemia.
conclusionsFuture 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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