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Endothelial-mesenchymal transition in atherosclerosis.

Celine Souilhol1, Martin C Harmsen2, Paul C Evans1

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Endothelial-mesenchymal transition (EndMT) contributes to atherosclerosis by enabling endothelial cells to become mesenchymal cells within plaques. Risk factors may promote EndMT, driving vascular disease progression.

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Area of Science:

  • Cardiovascular Biology
  • Cell Biology
  • Pathology

Background:

  • Atherosclerosis is an inflammatory arterial disease characterized by plaque formation.
  • The origin of mesenchymal cells within atherosclerotic plaques is a key research question.
  • Endothelial cells are increasingly recognized as a source of these plaque-associated mesenchymal cells.

Purpose of the Study:

  • To review the role of endothelial-mesenchymal transition (EndMT) in vascular disease, specifically atherosclerosis.
  • To describe the signaling pathways involved in EndMT during atherosclerosis.
  • To explore how atherosclerosis risk factors influence EndMT.

Main Methods:

  • Literature review focusing on endothelial-mesenchymal transition (EndMT) in atherosclerosis.
  • Analysis of current endothelial-lineage tracing studies.
  • Examination of biochemical and biomechanical signaling pathways.

Main Results:

  • Endothelial cells can undergo EndMT, losing endothelial markers and gaining mesenchymal characteristics.
  • EndMT facilitates the delamination and migration of endothelial cell-derived mesenchymal cells into tissues.
  • Systemic atherosclerosis risk factors are implicated in promoting EndMT.

Conclusions:

  • EndMT is a significant contributor to the mesenchymal cell population in atherosclerotic plaques.
  • Understanding EndMT pathways and risk factor contributions is crucial for targeting atherosclerosis.
  • Further research into EndMT mechanisms can offer new therapeutic strategies for vascular disease.