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In Silico Identification and Characterization of circRNAs During Host-Pathogen Interactions
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In Silico Identification and Characterization of circRNAs During Host-Pathogen Interactions

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Circular RNA profiling reveals an abundant circPTK2 that contributes everolimus-induced endothelial cell dysfunction

Yixin Zhao1, Jiangrong Wang1, Xiaomeng Jia1

  • 1Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, China.

Acta Cardiologica
|May 28, 2025
PubMed
Abstract

Insights

Circular RNA PTK2 (circPTK2) exacerbates endothelial dysfunction induced by everolimus, a drug-eluting stent component. Targeting the circPTK2/miR-1-5p/ACVR2B/StarD13 pathway may offer new treatments for in-stent restenosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Genomics

Background:

  • Drug-eluting stents (DESs) utilize mTOR inhibitors, which can promote in-stent neoatherosclerosis (ISNA) and late in-stent restenosis (ISR).
  • Circular RNAs (circRNAs) are implicated in various diseases, but their role in ISNA is not well understood.

Purpose of the Study:

  • To investigate the role of circRNAs in everolimus-induced endothelial dysfunction.
  • To elucidate the molecular mechanisms underlying circRNA involvement in ISNA.

Main Methods:

  • RNA sequencing to profile circRNAs in everolimus-treated human umbilical vein endothelial cells (HUVECs).
  • Quantitative real-time PCR to measure circRNA, miR-1-5p, and target gene expression.
  • Cellular assays (proliferation, migration, apoptosis, permeability) to assess circPTK2 function.
  • Bioinformatics, dual luciferase, and functional rescue experiments to determine molecular interactions.

Main Results:

  • CircPTK2 was significantly upregulated in everolimus-treated HUVECs.
  • CircPTK2 knockdown reversed everolimus-induced endothelial dysfunction, while overexpression worsened it.
  • CircPTK2 functions as a miR-1-5p sponge, upregulating ACVR2B and StarD13 expression.
  • Inflammatory conditions modulated the expression of circPTK2, miR-1-5p, and ACVR2B/StarD13.

Conclusions:

  • CircPTK2 plays a critical role in everolimus-induced endothelial dysfunction through the miR-1-5p/ACVR2B/StarD13 pathway.
  • This pathway represents a potential therapeutic target for late ISR following DES implantation.
Keywords:
CircPTK2Late in-stent restenosisMiR-1endothelial dysfunctioneverolimus-eluting stent

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