LncRNA ROR facilitates myocardial fibrosis in rats with viral myocarditis through regulating C-Myc expression

N Zhang1, Y Sun

  • 1Department of Internal Medicine-Cardiovascular, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, China. sunyao2121@163.com.

Abstract

Insights

Long non-coding RNA ROR exacerbates viral myocarditis and myocardial fibrosis in rats by up-regulating c-myc expression and increasing IL-6 levels. This promotes cardiac fibroblast proliferation and differentiation.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Virology

Background:

  • Viral myocarditis is a significant cause of heart disease.
  • Myocardial fibrosis is a key pathological feature of viral myocarditis.
  • The role of long non-coding RNAs (lncRNAs) in viral myocarditis remains incompletely understood.

Purpose of the Study:

  • To investigate the effect of lncRNA ROR on myocardial fibrosis in viral myocarditis.
  • To determine if lncRNA ROR regulates c-myc expression in this context.
  • To explore the potential therapeutic implications of targeting lncRNA ROR.

Main Methods:

  • Establishment of a viral myocarditis rat model.
  • Intervention with lncRNA ROR in a subset of rats.
  • Assessment of cardiac function (LVMI, LVW/TL, HMI), myocardial histology (HE and Masson staining), and molecular markers (c-myc, TGF-β, IL-6) via Western blotting, qRT-PCR, and ELISA.

Main Results:

  • Viral myocarditis rats showed increased cardiac mass indices and inflammatory cell infiltration.
  • lncRNA ROR intervention significantly worsened myocardial fibrosis, collagen deposition, and cardiac hypertrophy compared to the model group.
  • lncRNA ROR up-regulated the expression of c-myc, TGF-β, and serum IL-6 levels in myocardial tissues.

Conclusions:

  • lncRNA ROR plays a detrimental role in viral myocarditis by promoting myocardial fibrosis.
  • The mechanism involves up-regulation of c-myc expression and increased IL-6 levels.
  • lncRNA ROR facilitates cardiac fibroblast proliferation and differentiation, contributing to fibrosis.

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