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Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
Published on: July 3, 2018
Implication of microRNA as a potential biomarker of myocarditis
Jin-Hee Oh1, Gi Beom Kim2, Heeyoung Seok3
1Department of Pediatrics, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Abstract:
Myocarditis was previously attributed to an epidemic viral infection. Additional harmful reagents, in addition to viruses, play a role in its etiology. Coronavirus disease 2019 (COVID-19) vaccine-induced myocarditis has recently been described, drawing attention to vaccine-induced myocarditis in children and adolescents. Its pathology is based on a series of complex immune responses, including initial innate immune responses in response to viral entry, adaptive immune responses leading to the development of antigen-specific antibodies, and autoimmune responses to cellular injury caused by cardiomyocyte rupture that releases antigens. Chronic inflammation and fibrosis in the myocardium eventually result in cardiac failure. Recent advancements in molecular biology have remarkably increased our understanding of myocarditis. In particular, microRNAs (miRNAs) are a hot topic in terms of the role of new biomarkers and the pathophysiology of myocarditis. Myocarditis has been linked with microRNA-221/222 (miR-221/222), miR-155, miR-10a*, and miR-590. Despite the lack of clinical trials of miRNA intervention in myocarditis yet, multiple clinical trials of miRNAs in other cardiac diseases have been aggressively conducted to help pave the way for future research, which is bolstered by the success of recently U.S. Food and Drug Administration-approved small-RNA medications. This review presents basic information and recent research that focuses on myocarditis and related miRNAs as a potential novel biomarker and the therapeutics.
Insights
Myocarditis, including COVID-19 vaccine-associated cases, involves complex immune responses. MicroRNAs (miRNAs) show promise as biomarkers and therapeutic targets for myocarditis and related cardiac conditions.
Area of Science:
- Cardiology
- Immunology
- Molecular Biology
Background:
- Myocarditis etiology extends beyond viral infections to include other harmful agents.
- COVID-19 vaccine-associated myocarditis in pediatric populations highlights the need for further understanding.
- Pathology involves intricate immune responses, from innate and adaptive immunity to autoimmune reactions, potentially leading to cardiac failure.
Purpose of the Study:
- To review current knowledge on myocarditis, focusing on its pathophysiology and etiology.
- To explore the emerging role of microRNAs (miRNAs) as potential biomarkers and therapeutic targets in myocarditis.
- To discuss the implications of recent advancements in miRNA research for future myocarditis treatments.
Main Methods:
- Literature review of recent research on myocarditis and microRNAs.
- Analysis of the immunological pathways involved in myocarditis development.
- Examination of the role of specific microRNAs (e.g., miR-221/222, miR-155) in myocarditis.
Main Results:
- Myocarditis pathogenesis is complex, involving viral and non-viral triggers and multifaceted immune responses.
- Specific microRNAs, including miR-221/222, miR-155, miR-10a*, and miR-590, are associated with myocarditis.
- While direct clinical trials for miRNA intervention in myocarditis are pending, progress in other cardiac diseases and FDA-approved small-RNA therapies offer a positive outlook.
Conclusions:
- MicroRNAs represent a significant area of research for novel myocarditis biomarkers and therapeutic strategies.
- Understanding miRNA roles could lead to improved diagnostics and treatments for myocarditis and associated cardiac dysfunction.
- The success of miRNA-based therapies in other conditions supports their potential application in managing myocarditis.
Related Concept Videos
Myocarditis II: Clinical Features and Diagnostic Tests
Myocarditis I: Introduction
MicroRNAs
Myocarditis III: Medical Management
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