Contrasting Roles of Different Endoglin Forms in Atherosclerosis
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Endoglin (also known as CD105 or TGF-β type III receptor)is a co-receptor involved in TGF-β signaling. In atherosclerosis,TGF-β signaling is crucial in regulating diseaseprogression owing to its anti-inflammatory effects as well asits inhibitory effects on smooth muscle cell proliferation andmigration. Endoglin is a regulator of TGF-β signaling, but itsrole in atherosclerosis has yet to be defined. This review focuseson the roles of the various forms of endoglin inatherosclerosis. The expression of the two isoforms of endoglin(long-form and short-form) is increased in atheroscleroticlesions, and the expression of the soluble forms ofendoglin is upregulated in sera of patients with hypercholesterolemiaand atherosclerosis. Interestingly, long-formendoglin shows an atheroprotective effect via the inductionof eNOS expression, while short-form and soluble endoglinenhance atherogenesis by inhibiting eNOS expression andTGF-β signaling. This review summarizes evidence suggestingthat the different forms of endoglin have distinct roles inatherosclerosis.
Abstract
Endoglin (also known as CD105 or TGF-β type III receptor)is a co-receptor involved in TGF-β signaling. In atherosclerosis,TGF-β signaling is crucial in regulating diseaseprogression owing to its anti-inflammatory effects as well asits inhibitory effects on smooth muscle cell proliferation andmigration. Endoglin is a regulator of TGF-β signaling, but itsrole in atherosclerosis has yet to be defined. This review focuseson the roles of the various forms of endoglin inatherosclerosis. The expression of the two isoforms of endoglin(long-form and short-form) is increased in atheroscleroticlesions, and the expression of the soluble forms ofendoglin is upregulated in sera of patients with hypercholesterolemiaand atherosclerosis. Interestingly, long-formendoglin shows an atheroprotective effect via the inductionof eNOS expression, while short-form and soluble endoglinenhance atherogenesis by inhibiting eNOS expression andTGF-β signaling. This review summarizes evidence suggestingthat the different forms of endoglin have distinct roles inatherosclerosis.
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