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Targeting Circulating lncRNA ENST00000538705.1 Relieves Acute Coronary Syndrome via Modulating ALOX15

Hao Chen1, Shiwei Huang1, Fanlu Guan1

  • 1Department of Cardiology, The Third Affiliated Hospital of Shanghai University (Wenzhou People's Hospital), Wenzhou, 325000 Zhejiang, China.

Disease Markers
|May 16, 2022
PubMed
Abstract

Insights

Circulating ENST00000538705.1 promotes acute coronary syndrome (ACS) by regulating ALOX15. This study identifies potential therapeutic targets for ACS treatment, offering new avenues for managing this critical heart condition.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Biomarker Discovery

Background:

  • Acute coronary syndrome (ACS) represents a severe manifestation of coronary heart disease.
  • Identifying specific circulating biomarkers and their regulatory pathways is crucial for understanding ACS pathogenesis.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cardiovascular diseases.

Purpose of the Study:

  • To investigate ACS-specific circulating long non-coding RNAs (lncRNAs) and their regulatory mechanisms.
  • To identify novel molecular targets for the treatment of acute coronary syndrome.

Main Methods:

  • Serum samples from ACS patients and healthy controls underwent microarray analysis to identify dysregulated lncRNAs and mRNAs.
  • lncRNA-mRNA coexpression analysis was performed, followed by in vitro studies in human coronary artery endothelial cells (HCAECs) and in vivo experiments using myocardial infarction rat models.
  • Gene silencing via siRNA transfection was used to assess the functional roles of ENST00000538705.1 and ALOX15 in cellular processes and myocardial infarction.

Main Results:

  • Microarray analysis revealed 353 dysregulated lncRNAs and 441 dysregulated mRNAs in ACS patients.
  • ENST00000538705.1 was found to upregulate ALOX15 expression, and both were significantly elevated in ACS patients' serum.
  • Silencing ENST00000538705.1 or ALOX15 inhibited HCAEC proliferation and migration, reduced myocardial damage, and improved lipid profiles in a rat model of myocardial infarction.

Conclusions:

  • Circulating ENST00000538705.1 plays a critical role in promoting ACS progression by modulating ALOX15.
  • The ENST00000538705.1/ALOX15 axis represents a promising therapeutic target for acute coronary syndrome.
  • These findings contribute to the development of novel diagnostic and therapeutic strategies for ACS management.

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