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Differential Expression of Circulating Damage-Associated Molecular Patterns in Patients with Coronary Artery Ectasia

James N Tsoporis1, Andreas S Triantafyllis2,3, Andreas S Kalogeropoulos2,4

  • 1Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Unity Health Toronto, University of Toronto, 30 Bond St., Toronto, ON M5B 1W8, Canada.

Biomolecules
|January 26, 2024
PubMed

Insights

Coronary artery ectasia (CAE) involves abnormal coronary artery dilation. This study found increased damage-associated molecular patterns (DAMPs) and inflammatory markers in CAE patients, suggesting new diagnostic and therapeutic targets.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Molecular Biology

Background:

  • Coronary artery ectasia (CAE) is an abnormal dilation of coronary arteries, often coexisting with coronary artery disease (CAD).
  • The exact pathophysiology of CAE is unclear, but inflammation and damage-associated molecular patterns (DAMPs) are implicated.
  • DAMPs are endogenous molecules released from stressed tissues, acting as alarm signals for the innate immune system and promoting inflammation.

Purpose of the Study:

  • To investigate the differential expression of plasma DAMPs and related molecules in patients with CAE compared to those with CAD and healthy controls.
  • To explore the potential role of DAMPs as biomarkers and therapeutic targets in CAE.

Main Methods:

  • A prospective cross-sectional study involving 29 patients with CAE and non-obstructive CAD, 19 with obstructive CAD without CAE, and 14 matched controls.
  • Plasma levels of specific DAMPs (S100B, S100A12, HMGB1, HSP70), DAMPs receptors (TLR4, sRAGE), and miR328a-3p were measured.
  • An in vitro model using human umbilical vein endothelial cells was employed to assess inflammatory responses.

Main Results:

  • Patients with CAE exhibited significantly increased plasma levels of S100B, S100A12, HMGB1, HSP70, TLR4, and miR328a-3p compared to CAD and control groups.
  • Plasma levels of the antioxidant DJ-1 and the soluble form of the advanced glycation end product receptor (sRAGE) were decreased in both CAE and CAD groups compared to controls.
  • In vitro experiments confirmed that circulating DAMPs and CAE patient plasma induced inflammatory responses in endothelial cells.

Conclusions:

  • Differential expression of DAMPs (S100B, HSP70, HMGB1) and their receptors (TLR4, sRAGE) in CAE suggests their involvement in the disease's pathophysiology.
  • These DAMPs and their associated receptors represent promising novel biomarkers for CAE diagnosis.
  • The identified DAMPs may also serve as potential therapeutic targets for managing CAE.

Keywords:
DJ-1HSP70S100A12S100BTLR4coronary artery ectasiainflammationsRAGE

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