Pericardial Fluid of Patients With Coronary Artery Disease Can Drive Fibrosis Via TGF-Beta Pathway

Ali Fatehi Hassanabad1,2, Darrell D Belke2, Paul M K Gordon3

  • 1Section of Cardiac Surgery, Department of Cardiac Sciences, Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.

PubMed

Insights

Human pericardial fluid (PF) contains active markers that stimulate cardiac fibroblast activity via the transforming growth factor-beta pathway. This profibrotic capacity is elevated in patients with coronary artery disease.

Area of Science:

  • Cardiovascular biology
  • Fibrosis research
  • Biomarker discovery

Background:

  • Human pericardial fluid (PF) is a source of biologically active molecules.
  • Pericardial fluid influences cardiac cell behavior.
  • Transforming growth factor-beta (TGF-β) is a key regulator of fibrosis.

Purpose of the Study:

  • To investigate the role of acellular human pericardial fluid in cardiac fibroblast activation.
  • To identify the molecular pathways involved in PF-mediated fibroblast activity.
  • To compare the profibrotic capacity of PF from patients with and without coronary artery disease (CAD).

Main Methods:

  • In vitro assays using cardiac fibroblasts.
  • Analysis of acellular pericardial fluid.
  • Assessment of transforming growth factor-beta pathway activation.

Main Results:

  • The acellular component of human pericardial fluid promotes cardiac fibroblast activity in vitro.
  • This activation is mediated by the transforming growth factor-beta pathway.
  • Pericardial fluid from patients with coronary artery disease exhibits a significantly higher profibrotic capacity compared to that from control patients.

Conclusions:

  • Human pericardial fluid possesses intrinsic profibrotic properties.
  • The transforming growth factor-beta pathway is a critical mediator of PF-induced cardiac fibroblast activation.
  • Elevated profibrotic capacity of pericardial fluid in coronary artery disease patients may contribute to cardiac remodeling.

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