The role of endoglin in atherosclerosis
Language English Country Ireland Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
22460049
DOI
10.1016/j.atherosclerosis.2012.03.001
PII: S0021-9150(12)00158-X
Knihovny.cz E-resources
- MeSH
- Plaque, Atherosclerotic etiology MeSH
- Atherosclerosis physiopathology MeSH
- Atorvastatin MeSH
- Antigens, CD biosynthesis blood physiology MeSH
- Endothelium, Vascular MeSH
- Endoglin MeSH
- Hypercholesterolemia physiopathology MeSH
- Heptanoic Acids therapeutic use MeSH
- Humans MeSH
- Mice MeSH
- Swine MeSH
- Proteoglycans physiology MeSH
- Pyrroles therapeutic use MeSH
- Receptors, Cell Surface biosynthesis blood physiology MeSH
- Receptors, Transforming Growth Factor beta physiology MeSH
- Nitric Oxide Synthase Type III biosynthesis MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Atorvastatin MeSH
- betaglycan MeSH Browser
- Antigens, CD MeSH
- Endoglin MeSH
- ENG protein, human MeSH Browser
- Heptanoic Acids MeSH
- NOS3 protein, human MeSH Browser
- Proteoglycans MeSH
- Pyrroles MeSH
- Receptors, Cell Surface MeSH
- Receptors, Transforming Growth Factor beta MeSH
- Nitric Oxide Synthase Type 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.
References provided by Crossref.org
High Soluble Endoglin Levels Affect Aortic Vascular Function during Mice Aging
Long term effects of soluble endoglin and mild hypercholesterolemia in mice hearts
High soluble endoglin levels do not induce endothelial dysfunction in mouse aorta
