Related Experiment Video
Updated: Jul 8, 2026
Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
Programmed cell death in cardiac myocytes: strategies to maximize post-ischemic salvage
1Cardiovascular Research Center, Albert Einstein College of Medicine, Golding G-01, Morris Park Av., Bronx, NY 10461, USA. kmani@montefiore.org
Insights
Prior ischemic injury causes systolic dysfunction by reducing cardiac myocyte numbers. Cell death pathways like apoptosis and necrosis after myocardial infarction are key targets for future heart failure therapies.
Area of Science:
- Cardiology
- Cell Biology
- Pathophysiology
Background:
- Systolic dysfunction, often caused by ischemic injury, impacts cardiac myocyte numbers.
- Cardiac myocytes are central to myocardial pathogenesis and therapeutic strategies for ischemic syndromes.
Purpose of the Study:
- To review evidence of cell death in heart failure development post-myocardial infarction.
- To discuss relevant cell death pathways and potential therapeutic targets.
Main Methods:
- Literature review focusing on programmed cell death in myocardial infarction.
- Analysis of apoptosis, necrosis, and autophagic cell death mechanisms.
Main Results:
- Programmed cell death (apoptosis, necrosis, autophagic cell death) determines myocyte numbers post-myocardial infarction.
- Cell death is a critical factor in the progression of heart failure.
Conclusions:
- Understanding cell death pathways is crucial for developing novel therapies for heart failure.
- Targeting myocyte cell death offers a promising strategy to preserve cardiac function after myocardial infarction.
Abstract:
The most common cause of systolic dysfunction in the United States is prior ischemic injury. As the basic functional unit of the myocardium, the cardiac myocyte is the ultimate target of both the pathogenesis and possible therapies in this paradigm. Maintaining adequate numbers of these terminally differentiated units in the myocardium has been the focus of all therapies in ischemic syndromes, including reperfusion strategies. Programmed cell death, in the forms of apoptosis, necrosis and possibly, autophagic cell death are the final arbiters of myocyte numbers following myocardial infarction. This review will focus on the evidence for cell death in the development of heart failure following myocardial infarction, a brief review of the relevant pathways and the targets for development of future therapies.
