Urotensin-II and cardiovascular remodeling.

Abstract

Urotensin-II (U-II), a cyclic undecapeptide, and its receptor, UT, have been linked to vascular and cardiac remodeling. In patients with coronary artery disease (CAD), it has been shown that U-II plasma levels are significantly greater than in normal patients and the severity of the disease is increased proportionally to the U-II plasma levels. We showed that U-II protein and mRNA levels were significantly elevated in the arteries of patients with coronary atherosclerosis in comparison to healthy arteries. We observed U-II expression in endothelial cells, foam cells, and myointimal and medial vSMCs of atherosclerotic human coronary arteries. Recent studies have demonstrated that U-II acts in synergy with mildly oxidized LDL inducing vascular smooth muscle cell (vSMC) proliferation. Additionally, U-II has been shown to induce cardiac fibrosis and cardiomyocyte hypertrophy leading to cardiac remodeling. When using a selective U-II antagonist, SB-611812, we demonstrated a decrease in cardiac dysfunction including a reduction in cardiomyocyte hypertrophy and cardiac fibrosis. These findings suggest that U-II is undoubtedly a potential therapeutic target in treating cardiovascular remodeling.

• Authors: Panayiota Papadopoulos, Nicolas Bousette, Adel Giaid
• Journal: Peptides (Peptides) Vol. 29 Issue 5 Pg. 764-9 (May 2008) ISSN: 0196-9781 [Print] United States
• PMID: 17988761 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• SB-611812
• Sulfonamides
• Urotensins
• urotensin II

Topics

• Cardiovascular System (anatomy & histology, metabolism)
• Coronary Artery Disease (genetics, metabolism, pathology)
• Humans
• Sulfonamides (metabolism)
• Urotensins (antagonists & inhibitors, genetics, metabolism)
• Ventricular Remodeling (physiology)