Interventional Cardiology and
Angiology

Prevention of Restenosis - Molecular
basics
- The pathogenesis of the human restenotic lesions after
angioplasty is not well defined, but there is a consensus that
restenosis involves the interaction of cytokines, growth factors,
vascular and blood cellular elements, and the extent of
injury.
- The restenosis process can be divided into 3 or 4 phases:
- Thrombus formation, local inflammation, proliferation and
matrix formation.
- So far, the most pharmacological and interventional attempts
to reduce restenosis were focused on the reduction of thrombus
formation.
- Phase 3 proliferation:
- Local stimulation of cell proliferation: FGF, PDGF,
Thrombin, TGF-beta
- Phase 3 migration:
- Angiotensin II:
- AngII binds to G-protein-coupled AT1 receptor:
- Activation of phospholipase C and release of calcium,
stimulation of protein kinase C. Ang II stimulates also the
activity of phospholipase D.
- Activation of mitogen-activated protein kinase
- Regulation of c-fos expression
Universitätsklinikum Charité - Medizinische Fakultät
der Humboldt-Universität zu Berlin, Campus
Berlin-Buch
Franz-Volhard-Klinik
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Letzte Änderung: 17.11.98 -
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