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Galectin-3 mediates aldosterone-induced vascular fibrosis
Laurent Calvier1, Maria Miana, Pascal Reboul
1Inserm, U961, Faculty of Medicine, Université de Lorraine, Vandoeuvre-lès-Nancy, France.
Arteriosclerosis, Thrombosis, and Vascular Biology
|November 3, 2012
Summary
Galectin-3 (Gal-3) drives aldosterone-induced vascular fibrosis and inflammation. Inhibiting Gal-3 with modified citrus pectin or spironolactone reversed these effects in preclinical models.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Renal Physiology
Background:
- Aldosterone (Aldo) contributes to arterial stiffness and heart failure through unclear mechanisms.
- Galectin-3 (Gal-3), a lectin, is implicated in inflammation, fibrosis, and heart failure.
Purpose of the Study:
- To investigate the role of Gal-3 in aldosterone-induced vascular fibrosis.
Main Methods:
- Assessed Gal-3's effect on collagen synthesis in rat vascular smooth muscle cells.
- Utilized modified citrus pectin and small interfering RNA to inhibit Gal-3.
- Administered Aldo-salt to rats with spironolactone or modified citrus pectin.
- Treated wild-type and Gal-3 knock-out mice with Aldo.
Main Results:
- Gal-3 overexpression enhanced collagen type I synthesis; inhibition blocked Aldo-induced synthesis.
- Aldo-treated rats showed vascular hypertrophy, inflammation, fibrosis, and increased aortic Gal-3; treatments reversed these.
- Aldo increased aortic Gal-3, inflammation, and collagen type I in wild-type mice but not in Gal-3 knock-out mice.
Conclusions:
- Galectin-3 is essential for aldosterone-induced inflammatory and fibrotic responses in vascular smooth muscle cells.
- Gal-3 plays a critical role in mediating vascular fibrosis.
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