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Updated: Feb 6, 2026

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
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Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure

Published on: December 2, 2014

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Intravenous miR-144 reduces left ventricular remodeling after myocardial infarction

Jing Li1, Sean XiaoXiao Cai2, Quan He3

  • 1Division of Cardiology, Labatt Family Heart Center, Hospital for Sick Children, Toronto, ON, Canada.

Basic Research in Cardiology
|August 8, 2018
PubMed

Insights

MicroRNA-144 therapy significantly improved heart function and reduced scar size after myocardial infarction (MI) in mice. This cytoprotective microRNA (miRNA) shows potential for treating heart damage by reducing fibrosis, inflammation, and apoptosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Regenerative Medicine

Background:

  • MicroRNA-144 (miR-144) is a known cytoprotective microRNA.
  • Previous research demonstrated miR-144's acute cardioprotective effects in ischemia/reperfusion injury models.
  • The therapeutic potential of miR-144 in improving post-myocardial infarction (MI) cardiac remodeling remained to be fully elucidated.

Purpose of the Study:

  • To investigate the efficacy of miR-144 in improving cardiac remodeling in a non-reperfused myocardial infarction (MI) mouse model.
  • To assess the impact of miR-144 administration on cardiac function, infarct size, and associated pathological changes post-MI.

Main Methods:

  • Myocardial infarction was induced in C57BL/6 mice via permanent left anterior descending artery (LAD) ligation.
  • miR-144 was administered intravenously at varying doses (8-32 mg/kg) starting from day 0 post-MI, with repeated doses every 3 days until day 28.
  • Cardiac function was assessed using echocardiography and pressure-volume catheterization; infarct size, fibrosis, inflammation, and apoptosis were quantified.

Main Results:

  • Mice lacking miR-144 (miR-144 KO) exhibited exacerbated heart failure phenotypes, including ventricular dilation and impaired contractility.
  • Intravenous miR-144 administration significantly reduced infarct size and improved cardiac function, including LV fractional shortening, ejection fraction, and contractility indices (dP/dt max/min).
  • Beneficial effects were linked to reduced border zone fibrosis, inflammation, apoptosis, and modulated autophagy signaling, with miR-144 localized to cardiomyocytes and macrophages in the infarct area.

Conclusions:

  • Intravenous delivery of miR-144 demonstrates potent therapeutic effects on post-myocardial infarction remodeling.
  • miR-144 administration improves cardiac function and reduces adverse pathological changes following MI.
  • These findings highlight miR-144 as a promising therapeutic agent for treating myocardial infarction and its sequelae.
Keywords:
LAD, left anterior descending arteryMI, myocardial infarctionMiR, microRNAmTOR, mammalian target of rapamycin

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