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November 15, 2017JCI InsightOpen Access

Recapitulation of developmental mechanisms to revascularize the ischemic heart

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Key result

Following myocardial infarction in adult mice, de novo vessel formation occurs via reactivation of developmental mechanisms, including endocardial compaction and epicardial expansion, which are dependent on thymosin β4.

Population

Adult mice subjected to permanent ligation of the left anterior descending coronary artery to induce…

Comparison

Myocardial infarction and genetic lineage tracing. vs Sham-operated mice.

Design

Preclinical

Follow-up

Up to 14 days

Authors

KDKarina N. DubéTTTonia M. ThomasSMSonali Munshaw

Discussion

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Overview

May support thymosin β4 as a post-MI revascularization target; hypothesis-generating in mice and leaves open human translation.

Structured PICO

P
Population
Adult mice subjected to experimental myocardial infarction to investigate endogenous mechanisms of coronary neovascularization.
I
Intervention
Myocardial infarction (LAD ligation) and genetic lineage tracing.
C
Comparator
Sham-operated mice.
O
Outcome
Cellular sources and mechanisms of endogenous neovascularization after myocardial infarction.surrogate

The adult mouse heart reactivates developmental mechanisms, including endocardial compaction and coronary sinus sprouting, to revascularize ischemic tissue after myocardial infarction, highlighting potential therapeutic targets.

Limitations

  • The exact sources of endothelial cell contribution cannot be unambiguously delineated in the adult.
  • Definitive proof of endothelial-to-mesenchymal transition (EndMT) is currently lacking.

Cite This Study

Dubé et al. (2017) studied Myocardial infarction. Thymosin β4 knockout and genetic lineage tracing after myocardial infarction vs. Wild-type or sham-operated mice was evaluated on Endogenous neovascularization and epicardial/endocardial remodeling. Following myocardial infarction in adult mice, de novo vessel formation occurs via reactivation of developmental mechanisms, including endocardial compaction and epicardial expansion, which are dependent on thymosin β4.

synapsesocial.com/papers/6a9430ec189c14fbc5b95477https://doi.org/10.1172/jci.insight.96800
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