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[Atherosclerosis and oncogenes].

B Onraed-Dupriez1

  • 1Laboratoire de Biochimie, Hôpital Cardiologique, CHR de Lille, France.

Pathologie-Biologie
|January 1, 1992
PubMed
Summary
This summary is machine-generated.

Atherosclerosis may originate from a single cell, similar to benign tumors. Research suggests the sis oncogene and platelet-derived growth factor (PDGF) may drive this initial smooth muscle cell growth in atheroma plaques.

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Area of Science:

  • Cardiovascular Research
  • Oncology
  • Cell Biology

Context:

  • Atherosclerosis is a major cause of death, traditionally linked to lipids.
  • Benditt's monoclonal theory proposes atheroma plaques originate from a single smooth muscle cell, akin to a benign tumor.
  • Protooncogene activation is investigated as a mechanism for this monoclonal cell growth.

Purpose:

  • To explore the role of protooncogene activation in the earliest stages of atheroma plaque formation.
  • To investigate the potential link between the sis oncogene, platelet-derived growth factor (PDGF), and monoclonal smooth muscle cell proliferation in atherosclerosis.

Summary:

  • Recent research explores Benditt's monoclonal theory of atherosclerosis, suggesting plaques arise from a single cell.
  • Increased expression of the sis oncogene, which produces a protein similar to PDGF, has been observed in atheroma plaques.

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  • This finding complements existing theories by focusing on the initial cellular growth mechanisms driving plaque development.

    • Impact:

    • Shifts focus towards cellular mechanisms and oncogene involvement in atherosclerosis pathogenesis.
    • Provides a new perspective on atheroma plaque initiation, complementing lipid-centric theories.
    • Highlights potential therapeutic targets related to cell growth and oncogenes in cardiovascular disease.