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Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
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Microvesicles containing microRNA-21 induce myocardial fibrosis via AKT pathway

Y-W Xia1, S-B Wang

  • 1Department of Cardiovascular Medicine, Hanchuan City People's Hospital, Hanchuan, China. 1589885345@qq.com.

European Review for Medical and Pharmacological Sciences
|July 31, 2018
PubMed
Abstract

Insights

Microvesicles (MVs) containing microRNA-21 promote myocardial fibrosis by activating the AKT pathway. Inhibiting microRNA-21 expression alleviates fibrosis, suggesting a therapeutic target for heart disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biochemistry

Background:

  • Myocardial fibrosis is a significant contributor to heart failure.
  • Microvesicles (MVs) are implicated in intercellular communication and disease pathogenesis.
  • MicroRNA-21 (miR-21) is known to play roles in cardiac remodeling.

Purpose of the Study:

  • To investigate the role of microvesicles (MVs) carrying microRNA-21 (miR-21) in the development of myocardial fibrosis.
  • To elucidate the underlying molecular mechanisms, particularly the involvement of the AKT pathway.

Main Methods:

  • Established a rat model of myocardial ischemia to collect cardiac tissues.
  • Analyzed myocardial fibrosis indicators and miR-21 expression in both in vivo and in vitro models (TGF-β1 treated cardiomyocytes).
  • Utilized Western blot to detect AKT pathway-related genes and conducted rescue experiments using a miR-21 inhibitor.

Main Results:

  • Overexpression of MVs containing miR-21 was observed during myocardial fibrosis.
  • TGF-β1 treatment activated the AKT pathway in cardiomyocytes, correlating with fibrosis markers.
  • Inhibition of miR-21 significantly alleviated myocardial fibrosis in vitro.

Conclusions:

  • MVs carrying miR-21 promote myocardial fibrosis.
  • The pro-fibrotic effect is mediated through the activation of the AKT signaling pathway.
  • Targeting miR-21 within MVs presents a potential therapeutic strategy for myocardial fibrosis.

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