MIRNA-133A IN ACUTE MYOCARDIAL INFARCTION: MUCH MORE THAN A CARDIAC BIOMARKER

Abstract

Ischemic heart disease is a leading cause of morbidity and mortality worldwide. Infarct size
is the single most important predictor of adverse ventricular remodeling, and it is linearly dependent
upon the amount of myocardial salvage by reperfusion. Lack of timely reperfusion, due to ineffective
treatment or delayed presentation, leads to an unfavorable prognosis. Micro Ribo Nucleic Acids
(miRNAs) are small non-coding RNAs ~22 nucleotides in length that function as guide molecules in
RNA silencing. Targeting most protein-coding transcripts, miRNAs are involved in nearly all
developmental and pathological processes in animals. The biogenesis of miRNAs is under tight control,
and their dysregulation is associated with many human diseases. In cardiac diseases, including
myocardial infarction (MI), expression of cardiac miRNAs is markedly altered which leads to
deleterious effects associated with heart injury, arrhythmia, increased apoptosis, fibrosis, hypertrophy,
and tissue remodeling. In acute MI, circulating levels of cardiac miRNAs are significantly elevated
making them a promising diagnostic marker for early diagnosis of acute MI. The great cardio-specific
capacity of these miRNAs is very helpful for enhancing regenerative properties and survival of stem
cell and cardiac progenitor transplants and for reprogramming of mature non-cardiac cells to
cardiomyocytes. in this review we will illustrate the role of miRNA-133a in human heart and its
therapeutic implications.