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Updated: Jul 10, 2026

Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery

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Published on: August 16, 2019

Programmed cardiomyocyte death in myocardial infarction.

Hao Wu¹, Qi Lan¹, Yi-Xiang He¹

¹National Traditional Chinese Medicine Clinical Research Base, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, 646000, Sichuan, People's Republic of China.

Apoptosis : an International Journal on Programmed Cell Death

|January 20, 2025

Summary

Cardiovascular disease (CVD) causes heart failure (HF) after myocardial infarction (MI) due to cardiomyocyte death. Understanding programmed cell death (PCD) mechanisms offers new avenues for MI treatment and prevention.

Keywords:

Cardiac repair Cardiomyocytes Cardiovascular disease Myocardial infarction Programmed cell death

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Published on: March 30, 2022

Area of Science:

Cardiology
Cell Biology
Pathology

Background:

Cardiovascular disease (CVD) is a major global cause of mortality.
Myocardial infarction (MI) frequently leads to heart failure (HF) due to cardiomyocyte death.
Limited cardiomyocyte regeneration capacity exacerbates heart disease progression.

Purpose of the Study:

To explore the link between programmed cell death (PCD) in cardiomyocytes and MI.
To investigate the roles of apoptosis, necrosis, and autophagy in MI.
To assess the therapeutic potential of targeting PCD mechanisms for MI treatment.

Main Methods:

Literature review on cardiomyocyte death pathways.
Analysis of programmed cell death (PCD) mechanisms including apoptosis, necrosis, and autophagy.
Exploration of potential therapeutic strategies targeting these cell death pathways in myocardial infarction (MI).

Main Results:

Programmed cell death (PCD) pathways significantly contribute to cardiomyocyte loss during myocardial infarction (MI).
Apoptosis, necrosis, and autophagy play distinct roles in the pathogenesis of MI.
Targeting specific PCD mechanisms shows promise for mitigating MI-induced damage.

Conclusions:

Understanding cardiomyocyte death mechanisms is crucial for developing effective MI treatments.
Targeting apoptosis, necrosis, and autophagy could offer novel therapeutic strategies for heart failure (HF) post-MI.
Further research into PCD modulation may lead to improved prevention and treatment of myocardial infarction (MI).