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[Vascular aging. Role of elastin receptor]
1Laboratoire de Biologie Cellulaire, Paris.
Comptes Rendus Des Seances De La Societe De Biologie Et De Ses Filiales
|January 1, 1995
Summary
Arteriosclerosis, unlike atheromatous plaque, is age-dependent. Sustained elastin receptor activation by elastin peptides may initiate atherogenesis by impairing vascular health.
Area of Science:
- Cardiovascular Biology
- Vascular Medicine
- Biochemistry
Context:
- Arteriosclerosis and atheromatous plaque formation are distinct vascular processes.
- Lipid interactions with vascular wall constituents are implicated in both, via different mechanisms.
- Elastase activity and elastin peptide circulation increase with age, influencing arteriosclerosis progression.
Purpose:
- To differentiate between atheromatous plaque formation and arteriosclerosis.
- To elucidate the role of elastin peptides and receptor activation in vascular aging and atherogenesis.
- To propose a mechanism for the initiation of atherogenesis.
Summary:
- Arteriosclerosis is age-dependent, involving increased elastase activity and circulating elastin peptides.
- Sustained elastin receptor activation on endothelial cells produces nitric oxide (NO*) and superoxide, leading to peroxynitrite formation.
- Chronic oxidative stress and impaired vasorelaxation due to this process may initiate atherogenesis.
Impact:
- Highlights the critical role of elastin peptides in vascular aging.
- Suggests a novel pathway for the initiation of atheromatous plaque formation.
- Provides a potential therapeutic target for preventing atherosclerosis.