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The physiological role of endoglin in the cardiovascular system
José M López-Novoa1, Carmelo Bernabeu
1Instituto Reina Sofía de Investigación Nefrológica, Departamento de Fisiologia y Farmacologia, Universidad de Salamanca, and Red de Investigación Renal, Instituto de Salud Carlos III, Salamanca, Spain. jmlnovoa@usal.es
Insights
Endoglin (CD105), a key protein in blood vessel formation, plays a crucial role in vascular remodeling and angiogenesis. This review explores how different forms of endoglin regulate these processes and vascular tone.
Area of Science:
- Biochemistry
- Molecular Biology
- Vascular Biology
Background:
- Endoglin (CD105) is a glycoprotein acting as a coreceptor for TGF-β superfamily proteins.
- Mutations in endoglin cause hereditary hemorrhagic telangiectasia, a vascular malformation disease.
- Endoglin is crucial for angiogenesis, as shown by knockout mouse studies and its overexpression in tumors and inflammation.
Purpose of the Study:
- To review the role of different endoglin forms in angiogenesis, vascular remodeling, and vascular tone.
- To analyze the molecular and cellular mechanisms underlying endoglin's functions.
- To highlight endoglin's significance in vascular pathology and homeostasis.
Main Methods:
- Literature review of studies on endoglin's function.
- Analysis of genetic, cellular, and molecular data related to endoglin.
- Examination of endoglin's role in various physiological and pathological conditions.
Main Results:
- Endoglin is essential for proper angiogenesis and vascular development.
- Altered endoglin expression and function are linked to vascular diseases.
- Endoglin influences endothelial nitric oxide synthase, impacting vascular tone and angiogenesis.
Conclusions:
- Endoglin, in its various forms (long, short, soluble), is a critical regulator of vascular homeostasis.
- Understanding endoglin's mechanisms offers potential therapeutic targets for vascular disorders.
- Endoglin's multifaceted roles underscore its importance in vascular remodeling and angiogenesis.
Abstract:
Endoglin (CD105) is an integral membrane glycoprotein that serves as a coreceptor for members of the transforming growth factor-β superfamily of proteins. A major role for endoglin in regulating transforming growth factor-β-dependent vascular remodeling and angiogenesis has been postulated based on the following: 1) endoglin is the gene mutated in hereditary hemorrhagic telangiectasia type 1, a disease characterized by vascular malformations; 2) endoglin knockout mice die at midgestation because of defective angiogenesis; 3) endoglin is overexpressed in neoangiogenic vessels, during inflammation, and in solid tumors; and 4) endoglin regulates the expression and activity of endothelial nitric oxide synthase, which is involved in angiogenesis and vascular tone. Besides the predominant form of the endoglin receptor (long endoglin isoform), two additional forms of endoglin have been recently reported to play a role in the vascular pathology and homeostasis: the alternatively spliced short endoglin isoform and a soluble endoglin form that is proteolytically cleaved from membrane-bound endoglin. The purpose of this review is to underline the role that the different forms of endoglin play in regulating angiogenesis, vascular remodeling, and vascular tone, as well as to analyze the molecular and cellular mechanisms supporting these effects.
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