Recapitulation of developmental mechanisms to revascularize the ischemic heart.

Dubé KN, Thomas TM, Munshaw S, Rohling M, Riley PR, Smart N

JCI insight16 Nov 2017Cited by 64 (Europe PMC)

PMID29202457PMCIDPMC5752387DOI10.1172/jci.insight.96800PepBankPUB-29202457

Summary

Restoring blood flow after myocardial infarction (MI) is essential for survival of existing and newly regenerated tissue. Endogenous vascular repair processes are deployed following injury but are poorly understood. We sought to determine whether developmental mechanisms of coronary vessel formation are intrinsically reactivated in the adult mouse after MI. Using pulse-chase genetic lineage tracing, we establish that de novo vessel formation constitutes a substantial component of the neovascular response, with apparent cellular contributions from the endocardium and coronary sinus. The adult heart reverts to its former hypertrabeculated state and repeats the process of compaction, which may facilitate endocardium-derived neovascularization. The capacity for angiogenic sprouting of the coronary sinus vein, the adult derivative of the sinus venosus, may also reflect its embryonic origin. The quiescent epicardium is reactivated and, while direct cellular contribution to new vessels is minimal, it supports the directional expansion of the neovessel network toward the infarcted myocardium. Thymosin β4, a peptide with roles in vascular development, was required for endocardial compaction, epicardial vessel expansion, and smooth muscle cell recruitment. Insight into pathways that regulate endogenous vascular repair, drawing on comparisons with development, may reveal novel targets for therapeutically enhancing neovascularization.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

No result from this study comes from a test of the peptide.

Natural levels measured3

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

01AnimalEndogenous levelAnimal study (in vivo)Mechanism
In adult mice after myocardial infarction, the body's own thymosin β4 was required for endocardial compaction.
In plain wordsIn mice after a heart attack, the body's own thymosin β4 was needed for the inner heart lining to compact.
Peptide
Thymosin beta-4 (human)
Outcome
Not applicableEndocardial compaction after MI
Study
mousen: not reported in source
Myocardial infarction (MI)
Outcome group
Heart repair and regeneration · Cardiovascular
Source sentences
Summary
Thymosin β4, a peptide with roles in vascular development, was required for endocardial compaction, epicardial vessel expansion, and smooth muscle cell recruitment.
1 context sentence(design, population, supporting numbers)
Summary · context
We sought to determine whether developmental mechanisms of coronary vessel formation are intrinsically reactivated in the adult mouse after MI.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-2920245701
02AnimalEndogenous levelAnimal study (in vivo)Mechanism
In adult mice after myocardial infarction, the body's own thymosin β4 was required for epicardial vessel expansion.
In plain wordsIn mice after a heart attack, the body's own thymosin β4 was needed for new vessels to grow over the heart surface.
Peptide
Thymosin beta-4 (human)
Outcome
Not applicableEpicardial vessel expansion after MI
Study
mousen: not reported in source
Myocardial infarction (MI)
Outcome group
Heart repair and regeneration · Cardiovascular
Source sentences
Summary
Thymosin β4, a peptide with roles in vascular development, was required for endocardial compaction, epicardial vessel expansion, and smooth muscle cell recruitment.
1 context sentence(design, population, supporting numbers)
Summary · context
We sought to determine whether developmental mechanisms of coronary vessel formation are intrinsically reactivated in the adult mouse after MI.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-2920245702
03AnimalEndogenous levelAnimal study (in vivo)Mechanism
In adult mice after myocardial infarction, the body's own thymosin β4 was required for smooth muscle cell recruitment.
In plain wordsIn mice after a heart attack, the body's own thymosin β4 was needed to bring smooth muscle cells to new vessels.
Peptide
Thymosin beta-4 (human)
Outcome
Not applicableSmooth muscle cell recruitment after MI
Study
mousen: not reported in source
Myocardial infarction (MI)
Outcome group
Heart repair and regeneration · Cardiovascular
Source sentences
Summary
Thymosin β4, a peptide with roles in vascular development, was required for endocardial compaction, epicardial vessel expansion, and smooth muscle cell recruitment.
1 context sentence(design, population, supporting numbers)
Summary · context
We sought to determine whether developmental mechanisms of coronary vessel formation are intrinsically reactivated in the adult mouse after MI.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-2920245703

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
13 Oct 2026, 01:52 UTC
Study results updated
Version 1
12 Oct 2026, 18:17 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.