Inhibitory effect of microRNA-21 on pathways and mechanisms involved in cardiac fibrosis development

Cardiac fibrosis is a pivotal cardiovascular disease (CVD) process and represents a notable health concern worldwide. While the complex mechanisms underlying CVD have been widely investigated, recent research has highlighted microRNA-21's (miR-21) role in cardiac fibrosis pathogenesis. In this...

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Published in:Therapeutic advances in cardiovascular disease Vol. 18; p. 17539447241253134
Main Authors: Khalaji, Amirreza, Mehrtabar, Saba, Jabraeilipour, Armin, Doustar, Nadia, Rahmani Youshanlouei, Hamed, Tahavvori, Amir, Fattahi, Payam, Alavi, Seyed Mohammad Amin, Taha, Seyed Reza, Fazlollahpour-Naghibi, Andarz, Shariat Zadeh, Mahdieh
Format: Journal Article
Language:English
Published: England SAGE Publishing 01-01-2024
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Summary:Cardiac fibrosis is a pivotal cardiovascular disease (CVD) process and represents a notable health concern worldwide. While the complex mechanisms underlying CVD have been widely investigated, recent research has highlighted microRNA-21's (miR-21) role in cardiac fibrosis pathogenesis. In this narrative review, we explore the molecular interactions, focusing on the role of miR-21 in contributing to cardiac fibrosis. Various signaling pathways, such as the RAAS, TGF-β, IL-6, IL-1, ERK, PI3K-Akt, and PTEN pathways, besides dysregulation in fibroblast activity, matrix metalloproteinases (MMPs), and tissue inhibitors of MMPs cause cardiac fibrosis. Besides, miR-21 in growth factor secretion, apoptosis, and endothelial-to-mesenchymal transition play crucial roles. miR-21 capacity regulatory function presents promising insights for cardiac fibrosis. Moreover, this review discusses numerous approaches to control miR-21 expression, including antisense oligonucleotides, anti-miR-21 compounds, and Notch signaling modulation, all novel methods of cardiac fibrosis inhibition. In summary, this narrative review aims to assess the molecular mechanisms of cardiac fibrosis and its essential miR-21 function.
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ISSN:1753-9447
1753-9455
DOI:10.1177/17539447241253134