Related Experiment Video
Updated: Sep 10, 2025

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Noncoding RNAs in myocardial ischemia/reperfusion injury and repair
Mingliang Pan1,2, Zhixin Li2, Xiaohong Wang2
1Department of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Abstract:
Myocardial ischemia/reperfusion (I/R) usually triggers a series of molecular and cellular changes, which yield excessive oxidative stress and massive cardiomyocyte death, leading to sterile inflammation, cardiac fibrosis, and, eventually, heart failure. Over the past two decades, numerous studies have demonstrated that noncoding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), involve almost every aspect of adverse cardiac remodeling induced by I/R. They have emerged as key regulators in the process of cardiac cell death (i.e. apoptosis, necroptosis, ferroptosis, pyroptosis, and PANoptosis), fibrosis, angiogenesis, and immune responses during myocardial I/R. Herein, this review summarizes recent advancements on ncRNA-mediated regulation of cardiac cell death, cardiac angiogenesis, fibrosis, and macrophage function as well as intercellular communication following myocardial I/R. Finally, the therapeutic potential of ncRNAs for treating myocardial I/R injury and future research directions are also discussed.
Insights
Noncoding RNAs (ncRNAs) significantly regulate heart cell death, fibrosis, and immune responses after myocardial ischemia/reperfusion (I/R) injury. Targeting these ncRNAs offers promising therapeutic strategies for heart failure treatment.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- RNA Biology
Background:
- Myocardial ischemia/reperfusion (I/R) injury causes oxidative stress, cardiomyocyte death, and heart failure.
- Noncoding RNAs (ncRNAs) are critical regulators in cardiac remodeling following I/R.
- ncRNAs, including miRNAs, lncRNAs, and circRNAs, influence multiple pathological processes in the heart.
Purpose of the Study:
- To review recent advancements in ncRNA-mediated regulation of myocardial I/R injury.
- To summarize the role of ncRNAs in cardiac cell death, angiogenesis, fibrosis, and immune responses.
- To discuss the therapeutic potential of ncRNAs for I/R injury and future research directions.
Main Methods:
- Literature review of studies on ncRNAs in myocardial I/R injury.
- Analysis of ncRNA involvement in cardiac cell death pathways (apoptosis, necroptosis, ferroptosis, pyroptosis, PANoptosis).
- Examination of ncRNA roles in cardiac fibrosis, angiogenesis, macrophage function, and intercellular communication.
Main Results:
- ncRNAs are key regulators of diverse cellular processes during myocardial I/R.
- Specific ncRNAs modulate cardiomyocyte death, inflammatory responses, and fibrotic remodeling.
- ncRNAs impact macrophage polarization and intercellular signaling in the injured heart.
Conclusions:
- ncRNAs play a central role in the molecular and cellular responses to myocardial I/R.
- Targeting ncRNAs presents a promising therapeutic avenue for mitigating I/R-induced heart damage.
- Further research into ncRNA mechanisms and therapeutic applications is warranted for treating heart failure.
More Related Videos
05:54Preparation of a Non-Cardiomyocyte Cell Suspension for Single-Cell RNA Sequencing from a Post-Myocardial Infarction Adult Mouse Heart
Published on: February 3, 2023
09:53Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
Related Concept Videos
Types of RNA
RNA Performs Diverse...
lncRNA - Long Non-coding RNAs
RNA Interference
This process occurs naturally in cells, often through the activity of genomically-encoded microRNAs. Researchers can take advantage of this mechanism by introducing synthetic RNAs to deactivate specific genes for research or therapeutic purposes. For example, RNAi could be used...
Regulation of the Unfolded Protein Response
Myocarditis I: Introduction
Experimental RNAi