Abstract
At present, cardiovascular diseases are depicted to be the leading cause of death worldwide according to the World Health Organization. In the future, projections predict that ischemic heart disease will persist in the top main causes of illness. Within this alarming context, some tiny master regulators of gene expression programs, namely, microRNAs (miRNAs) carry three promising potentials. In fact, miRNAs can prove to be useful not only in terms of biomarkers allowing heart injury detection but also in terms of therapeutics to overcome limitations of past strategies and treat the lesions. In a more creative approach, they can even be used in the area of human engineered cardiac tissues as maturation tools for cardiomyocytes (CMs) derived from pluripotent stem cell. Very promising not only for patient-specific cell-based therapies but also to develop biomimetic microsystems for disease modeling and drug screening, these cells greatly contribute to personalized medicine. To get into the heart of the matter, the focus of this review lies primarily on miRNAs as acute myocardial infarction (AMI) biomarkers. Only large cohort studies comprising over 100 individuals to reach a potent statistical value were considered. Certain miRNAs appeared to possibly complement protein-based biomarkers and classical risk factors. Some were even described to bear potential in the discrimination of similar symptomatic pathologies. However, differences between pre-analytical and analytical approaches substantially influenced miRNA data. Further supported by meta-analysis studies, this problem had to be addressed. A detailed critical analysis of each step to define miRNAs biomarker potential is provided to inspire a future improved universal strategy. Interestingly, a recurrent set of cardiomyocyte-enriched miRNAs was found, namely, miR-1; miR-133; miR-208a/b; and miR-499a. Each member of this myomiRs group displayed promising roles either individually or in combination as AMI diagnostic or prognostic biomarkers. Furthermore, a precise combo was shown to be powerful enough to transdifferentiate human fibroblasts into CMs opening doors in the therapeutics. Following these discoveries, they also emerged as optional tools to transfect in order to mature CMs derived from pluripotent stem cells. Ultimately, the multiple potentials carried by the myomiRs miR-1; miR-133; miR-208a/b; and miR-499a still remain to be fully unveiled.
Highlights
Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality in industrialized countries and their incidence are in constant increase due to the progressive aging of population (1)
CVDs can be of multiple order and numerous insults can cause them, including ischemia, hypertension, genetic mutations among others, and they are often associated with loss or dysfunction of cardiac muscle cells, diminished pump function, and arrhythmias
In a multiple linear regression analysis that included clinical variables and, hs-cardiac troponin T (cTnT) detected by immunoassay and myomiRs detected by real-time polymerase chain reaction (qPCR), results showed an independent association
Summary
Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality in industrialized countries and their incidence are in constant increase due to the progressive aging of population (1). CVDs can be of multiple order and numerous insults can cause them, including ischemia, hypertension, genetic mutations among others, and they are often associated with loss or dysfunction of cardiac muscle cells, diminished pump function, and arrhythmias. Cardiac muscle is composed of myocyte and non-myocyte cells and an extracellular matrix involved in the cohesion of the all tissue. Even if cardiomyocytes (CMs) cover approximately 75% of the myocardial volume, they only represent nearly 20–30% of the cell population (2). Despite of long being described as cells unable to renew, cardiac muscle cells can regenerate. Once damaged, the adult human heart cannot heal completely, leading to cardiac insufficiency and heart failure
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