• Grażyna Sygitowicz, Agata Maciejak-Jastrzębska, and Dariusz Sitkiewicz.
• Department of Clinical Chemistry and Laboratory Diagnostics, Medical University of Warsaw, Warsaw, Poland. gsygitowicz@poczta.onet.pl
• Pol. Arch. Med. Wewn. 2020 Jan 31; 130 (1): 59-65.

AbstractAcute myocardial infarction (AMI) induces unfavorable left ventricular remodeling (LVR), a complex process that involves molecular, cellular, and geometric alterations leading to important changes in heart structure and function. Heart failure (HF) is a frequent complication of AMI, and it remains a serious clinical, epidemiological, and economic challenge. Despite advances in the therapy and management of HF, many patients still suffer from severe symptoms. The underlying molecular mechanisms of the post‑AMI LVR are not yet fully understood. Numerous studies have indicated that dysregulation in the expression of microRNA (miRNA) molecules leads to changes in several pathological processes in the heart, which are associated with post‑AMI transition from cardiac hypertrophy to HF. In this review, we summarize the current knowledge on the role of miRNAs in the regulation of basic processes, such as excessive myocardial fibrosis, pathological cardiomyocyte hypertrophy, and myocardial cell apoptosis. Moreover, the significance of circulating miRNAs as noninvasive prognostic biomarkers in the prediction of LVR and HF after AMI has also been discussed. In conclusion, miR‑29 family members (miR‑29a and miR‑29b), miR‑150, and miR‑30a‑5p represent different groups of miRNAs, but all of them are involved in the regulation of the fundamental processes associated with post‑AMI left ventricular dysfunction and HF. Furthermore, these miRNA molecules may serve as a potential therapeutic target during disease progression.

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