The role of endoglin in atherosclerosis
Jazyk angličtina Země Irsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
22460049
DOI
10.1016/j.atherosclerosis.2012.03.001
PII: S0021-9150(12)00158-X
Knihovny.cz E-zdroje
- MeSH
- aterosklerotický plát etiologie MeSH
- ateroskleróza patofyziologie MeSH
- atorvastatin MeSH
- CD antigeny biosyntéza krev fyziologie MeSH
- cévní endotel MeSH
- endoglin MeSH
- hypercholesterolemie patofyziologie MeSH
- kyseliny heptylové terapeutické užití MeSH
- lidé MeSH
- myši MeSH
- prasata MeSH
- proteoglykany fyziologie MeSH
- pyrroly terapeutické užití MeSH
- receptory buněčného povrchu biosyntéza krev fyziologie MeSH
- receptory transformujícího růstového faktoru beta fyziologie MeSH
- synthasa oxidu dusnatého, typ III biosyntéza MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- atorvastatin MeSH
- betaglycan MeSH Prohlížeč
- CD antigeny MeSH
- endoglin MeSH
- ENG protein, human MeSH Prohlížeč
- kyseliny heptylové MeSH
- NOS3 protein, human MeSH Prohlížeč
- proteoglykany MeSH
- pyrroly MeSH
- receptory buněčného povrchu MeSH
- receptory transformujícího růstového faktoru beta MeSH
- synthasa oxidu dusnatého, typ III MeSH
Endoglin (CD 105, TGF-β receptor III) is a homodimeric transmembrane glycoprotein that plays a regulatory role in TGF-β signaling. Its functional role in the context of atherosclerosis has yet to be defined and should be stated here. Therefore, we focused on the role of endoglin in atherosclerosis in both humans and experimental animals. Endoglin expression was demonstrated in atherosclerotic vessels predominantly in endothelial cells and smooth muscle cells in various types of blood vessels in mice and humans, suggesting its participation in atherogenesis. Endoglin expression was also related to the expression of eNOS in endothelium, repair of the vessel wall, plaque neoangiogenesis, production of collagen and stabilization of atherosclerotic lesions. In addition, increased levels of soluble endoglin were associated with hypercholesterolemia, atherosclerosis, acute myocardial infarction and were related to inhibition of TGF-β signaling in the vessel wall. Moreover, soluble endoglin levels were significantly lowered after a series of extracorporeal eliminations in patients with familial hypercholesterolemia. Additionally, statin treatment decreased levels of soluble endoglin and increased its expression in aorta, which was related to reduced atherosclerosis in mice. In conclusion, we propose that measurement of soluble endoglin might give information about progression of the atherosclerotic process or the efficacy of therapeutic interventions, which is the task that must be answered in clinical trials.
Citace poskytuje Crossref.org
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Long term effects of soluble endoglin and mild hypercholesterolemia in mice hearts
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