Why the study?
Immediately postnatal mammalian hearts can regenerate after infarction, but the cells, pathways, and molecules regulating this behavior remain unclear.
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Population
Regenerative and older nonregenerative mouse hearts
Comparison
Regenerative vs older nonregenerative mouse hearts
Design
Comparative RNA-Seq dataset analysis
Answers are grounded in this paper and cite their sources.
May flag day-3 inflammation as linked to adult post-MI fibrosis; leaves open macrophage-targeted strategies to restore regeneration.
Immediately postnatal mammalian hearts are able to regenerate after infarction, but the cells, pathways, and molecules that regulate this behavior are unclear. By comparing RNA-Seq datasets from regenerative mouse hearts and older, nonregenerative hearts, we are able to identify biological processes that are hallmarks of regeneration. We find that sterile inflammatory processes are upregulated in nonregenerative hearts, initiating profibrotic gene programs 3 days after myocardial infarction that can cause myocardial disease.
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Whitehead et al. (2021) studied this question.
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