Related Experiment Video
Updated: Feb 10, 2026
09:05
In Vitro and In Vivo Models to Study Corneal Endothelial-mesenchymal Transition
Published on: August 20, 2016
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Endothelial-to-Mesenchymal Transition in Post-Myocardial Infarction Fibrosis: A Maladaptive but Targetable Pathway
1Department of Biomedical Engineering, University of Massachusetts Amherst, Amherst, USA.
EJIFCC
|February 9, 2026
Summary
Endothelial-to-mesenchymal transition (EndMT) drives maladaptive heart scarring after myocardial infarction (MI). Targeting EndMT pathways offers a precision strategy to improve outcomes by limiting fibrosis and preserving blood vessels.
Area of Science:
- Cardiovascular Research
- Fibrosis Mechanisms
- Regenerative Medicine
Background:
- Myocardial infarction (MI) triggers scar formation, crucial for healing but can lead to maladaptive fibrosis and heart failure.
- Established antifibrotic therapies have limited success due to the dual role of fibroblasts in scar integrity and fibrosis.
- Endothelial-to-mesenchymal transition (EndMT) is an underappreciated contributor to post-MI fibrosis.
Purpose of the Study:
- To review the role of EndMT in post-myocardial infarction (MI) fibrosis.
- To highlight EndMT as a distinct, maladaptive contributor to cardiac fibrosis.
- To explore therapeutic strategies targeting EndMT for improved MI outcomes.
Main Methods:
- Review of experimental studies on EndMT in post-MI cardiac remodeling.
- Analysis of evidence for EndMT in human ischemic cardiomyopathy.
- Examination of regulatory pathways and potential therapeutic targets of EndMT.
Main Results:
- EndMT contributes 10-30% of fibroblast-like cells post-MI, promoting fibrosis without improving scar strength.
- EndMT leads to microvascular rarefaction and impaired perfusion, unlike beneficial fibroblast activity.
- EndMT is regulated by specific pathways (e.g., TGF-β, Notch, Wnt) and shows partial reversibility.
Conclusions:
- EndMT represents a maladaptive fibrotic process in the adult heart after MI.
- Targetable pathways regulating EndMT offer opportunities for time-limited, pathway-specific interventions.
- Biomarker-guided, EndMT-directed therapies hold promise for precision treatment to limit fibrosis and improve cardiac function post-MI.
Keywords:
Anti-fibrotic TherapyBiomarkersCardiac FibrosisEndothelial-to-Mesenchymal Transition (EndMT)Myocardial InfarctionTGF-β SignalingTranslational CardiologyMore Related Videos
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