Abstract
Recent knowledge concerning the role of non-coding RNAs (ncRNAs) in myocardial ischemia/reperfusion (I/R) injury provides new insight into their possible roles as specific biomarkers for early diagnosis, prognosis, and treatment. MicroRNAs (miRNAs) have fewer than 200 nucleotides, while long ncRNAs (lncRNAs) have more than 200 nucleotides. The three types of ncRNAs (miRNAs, lncRNAs, and circRNAs) act as signaling molecules strongly involved in cardiovascular disorders (CVD). I/R injury of the heart is the main CVD correlated with acute myocardial infarction (AMI), cardiac surgery, and transplantation. The expression levels of many ncRNAs and miRNAs are highly modified in the plasma of MI patients, and thus they have the potential to diagnose and treat MI. Cardiomyocyte and endothelial cell death is the major trigger for myocardial ischemia–reperfusion syndrome (MIRS). The cardioprotective effect of inflammasome activation in MIRS and the therapeutics targeting the reparative response could prevent progressive post-infarction heart failure. Moreover, the pharmacological and genetic modulation of these ncRNAs has the therapeutic potential to improve clinical outcomes in AMI patients.
Highlights
Myocardial ischemia–reperfusion (I/R) injury in acute myocardial infarction (AMI) is the most important cause of morbidity and mortality worldwide [1]
myocardial infarction-associated transcript (MIAT) acts as a pro-hypertrophic long ncRNAs (lncRNAs) in cardiomyocytes by sponging the anti-hypertrophic miR-150, miR-93, and miR-93 via TLR4
NcRNAs are ubiquitous RNA molecules that play a key role in modulating the molecular mechanisms underlying the pathogenesis of cardiovascular diseases
Summary
Myocardial ischemia–reperfusion (I/R) injury in acute myocardial infarction (AMI) is the most important cause of morbidity and mortality worldwide [1]. The exact mechanisms through which the homeostasis of myocardial cells is affected during I/R injury of the heart are not completely understood [2] Pathological changes such as inflammation, autophagy, apoptosis, calcium overload, neurohumoral activation, and oxidative stress are considered to have the same underlying cause as I/R injury [3]. The human genome is transcribed into various classes of functional non-coding RNAs that are powerful regulators of a multitude of cellular and pathological processes [7]. Based on their size, molecules have fewer than 200 nucleotides for short non-coding RNAs including microRNAs (miRNAs), while long ncRNAs (lncRNAs) have more than 200 nucleotides. While the ischemic area expands according to the duration and severity of blood flow reduction, maximum reperfusion is achieved in a moderate ischemic injury [4,6,7]
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