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A Modified Simple Method for Induction of Myocardial Infarction in Mice
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Myocardial infarction induces endothelial dysfunction with independence of cardiovascular risk factors

Francisco Rafael Jimenez-Trinidad1, Núria Solanes1, Marta Arrieta1

  • 1Cardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.

Angiogenesis
|October 1, 2025
PubMed

Insights

Myocardial infarction (MI) causes lasting endothelial colony-forming cell (ECFC) dysfunction, independent of cardiovascular risk factors. Targeting the MSK2/MKK3/p53 pathway may restore endothelial function and improve angiogenesis post-MI.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Biology
  • Ischemic Heart Disease Research

Background:

  • Endothelial dysfunction and impaired angiogenesis are key features of ischemic heart disease.
  • Myocardial infarction (MI) significantly impacts cardiovascular outcomes.
  • The direct effect of MI on endothelial function, independent of cardiovascular risk factors (CVRFs), is not fully understood.

Purpose of the Study:

  • To investigate the direct impact of MI on endothelial function.
  • To utilize human and porcine endothelial colony-forming cells (ECFCs) as a model to assess MI-induced endothelial dysfunction.
  • To determine if MI triggers endothelial dysfunction independently of CVRFs.

Main Methods:

  • Isolated human ECFCs (hECFCs) from healthy volunteers, patients immediately after MI (AMI), and 6 months post-MI (CMI).
  • Established a porcine model of MI, isolating porcine ECFCs (pECFCs) before and 1 month after MI (CMI).
  • Assessed ECFC colony formation, morphology, senescence, oxidative stress, proliferation, migration, and the MSK2/MKK3/p53 signaling pathway.

Main Results:

  • CMI-hECFCs and CMI-pECFCs showed delayed colony formation; AMI-hECFCs did not.
  • AMI-hECFCs and CMI-hECFCs exhibited morphological changes; CMI-pECFCs showed shape changes.
  • Senescence increased in AMI-hECFCs and CMI-hECFCs; oxidative stress elevated only in CMI-hECFCs.
  • Angiogenic and proliferative capacities were reduced in all MI-affected ECFCs; migration impaired in CMI-hECFCs and CMI-pECFCs.
  • Overactivation of the MSK2/MKK3/p53 axis was observed in dysfunctional ECFCs.

Conclusions:

  • Myocardial infarction induces persistent ECFC dysfunction, independent of CVRFs.
  • The MSK2/MKK3/p53 signaling pathway is implicated in MI-induced ECFC dysfunction.
  • Inhibiting the MSK2/MKK3/p53 pathway offers a potential therapeutic strategy for improving endothelial function and angiogenesis post-MI.
Abstract

Keywords:
AngiogenesisEndothelial cellsMAPKMyocardial infarctionRisk factors

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