Why the study?
Myocardial infarction and subsequent unfavorable remodeling cause high mortality and heart failure, urgently warranting therapies targeting ncRNAs to limit atherosclerotic plaque progression, cardiac damage, and remodeling.
Targeting non-coding RNAs represents a potential future therapeutic option for limiting atherosclerotic plaque progression, cardiac damage during myocardial infarction, and subsequent remodeling.
Supports investigation of therapies targeting plaque progression and post-MI remodeling; leaves open clinical validation in trials.
Myocardial infarction is one of the major causes of mortality worldwide and is a main cause of heart failure. This disease appears as a final point of atherosclerotic plaque progression, destabilization, and rupture. As a consequence of cardiomyocytes death during the infarction, the heart undergoes unfavorable cardiac remodeling, which results in its failure. Therefore, therapies aimed to limit the processes of atherosclerotic plaque progression, cardiac damage during the infarction, and subsequent remodeling are urgently warranted. A hopeful therapeutic option for the future medicine is targeting and regulating non-coding RNA (ncRNA), like microRNA, circular RNA (circRNA), or long non-coding RNA (lncRNA). In this review, the approaches targeted at ncRNAs participating in the aforementioned pathophysiological processes involved in myocardial infarction and their outcomes in preclinical studies have been concisely presented.
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Kowara et al. (2021) studied this question.
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