Contrasting roles of different endoglin forms in atherosclerosis

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• Cell Signaling

Background:

• Endoglin (CD105) is a TGF-β type III receptor crucial for TGF-β signaling.
• TGF-β signaling impacts atherosclerosis by modulating inflammation and smooth muscle cell behavior.
• The specific role of endoglin in atherosclerosis remains to be fully elucidated.

Purpose of the Study:

• To review the distinct roles of endoglin isoforms and soluble forms in atherosclerosis.
• To analyze how endoglin influences TGF-β signaling and eNOS expression in the context of atherosclerosis.
• To synthesize current evidence on endoglin's multifaceted impact on atherosclerotic disease progression.

Main Methods:

• Literature review focusing on endoglin expression and function in atherosclerosis.
• Analysis of studies examining long-form, short-form, and soluble endoglin.
• Evaluation of endoglin's effects on eNOS expression and TGF-β signaling pathways.

Main Results:

• Both long-form and short-form endoglin expression increase in atherosclerotic lesions.
• Soluble endoglin levels are elevated in hypercholesterolemia and atherosclerosis patients.
• Long-form endoglin exhibits atheroprotective effects by inducing eNOS; short-form and soluble endoglin promote atherogenesis by inhibiting eNOS and TGF-β signaling.

Conclusions:

• Different endoglin forms exert opposing effects on atherosclerosis.
• Long-form endoglin is atheroprotective, whereas short-form and soluble endoglin are pro-atherogenic.
• Endoglin's distinct roles highlight its complex involvement in cardiovascular disease pathogenesis.