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Elastin fragmentation and atherosclerosis progression: the elastokine concept
Pascal Maurice1, Sébastien Blaise, Stéphanie Gayral
1Laboratoire Signalisation et Récepteurs Matriciels (SiRMa), FRE CNRS 3481 MEDyC, Université de Reims Champagne Ardenne, Faculté des Sciences Exactes et Naturelles, Reims, France.
Trends in Cardiovascular Medicine
|April 9, 2013
Summary
Atherosclerosis involves arterial plaque buildup and inflammation. Elastin-derived peptides, released from degraded elastin, accelerate disease progression via the elastin receptor complex (ERC), a potential therapeutic target.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Atherosclerosis is a complex inflammatory arterial disease.
- Vascular extracellular matrix degradation and remodeling are key features.
- Elastin, crucial for arterial elasticity, is degraded by elastases, producing elastin-derived peptides (EDP).
Purpose of the Study:
- To review elastin's role in atherosclerosis progression.
- To examine the biological processes influenced by elastin degradation.
- To discuss the elastin receptor complex (ERC) as a therapeutic target.
Main Methods:
- Literature review of studies on elastin, EDP, and atherosclerosis.
- Analysis of the mechanisms by which EDP influence disease progression.
- Evaluation of the elastin receptor complex (ERC) and its signaling pathways.
Main Results:
- Elastin degradation by elastases releases EDP.
- EDP actively promote atherosclerosis by accelerating LDL oxidation and vascular calcification.
- EDP exert their effects through binding to the elastin receptor complex (ERC).
Conclusions:
- Elastin plays a significant role in atherosclerosis pathogenesis.
- The elastin receptor complex (ERC) and its signaling pathways are promising therapeutic targets for atherosclerosis.
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