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MicroRNA-378 attenuates myocardial fibrosis by inhibiting MAPK/ERK pathway

W-Y Liu1, H-H Sun, P-F Sun

  • 1Department of Cardiovascular Surgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. spfsunny@126.com.

European Review for Medical and Pharmacological Sciences
|June 8, 2019
PubMed
Abstract

Insights

MicroRNA-378-containing microvesicles (MVs) alleviate myocardial fibrosis by inhibiting the MAPK pathway. Reduced MV levels worsen fibrosis, highlighting their protective role.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biochemistry

Background:

  • Myocardial fibrosis (MF) is a pathological process contributing to heart dysfunction.
  • Microvesicles (MVs) are emerging as key mediators in intercellular communication.
  • MicroRNA-378's role in cardiovascular disease requires further elucidation.

Purpose of the Study:

  • To investigate the function of microRNA-378-containing microvesicles (MVs) in myocardial fibrosis.
  • To explore the underlying molecular mechanisms involving the mitogen-activated protein kinase (MAPK) pathway.

Main Methods:

  • Established a rat model of chronic myocardial fibrosis via aortic coarctation.
  • Administered microRNA-378 mimics or inhibitors and isolated MVs from cardiomyocytes.
  • Quantified fibrosis indicators, microRNA-378, and MAPK pathway activation using qRT-PCR and Western blot.

Main Results:

  • Decreased levels of microRNA-378-containing MVs were observed in the myocardial fibrosis model.
  • Activation of the MAPK pathway correlated with increased myocardial fibrosis.
  • MicroRNA-378-containing MVs were found to inhibit MAPK phosphorylation.

Conclusions:

  • MicroRNA-378-containing MVs play a protective role against myocardial fibrosis.
  • These MVs exert their effect by suppressing the phosphorylation of the MAPK pathway.
  • Targeting microRNA-378-containing MVs may offer a therapeutic strategy for myocardial fibrosis.

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