ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Alagebrium inhibits neointimal hyperplasia and restores distributions of wall shear stress by reducing downstream vascular resistance in obese and diabetic rats.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Age-related arterial stiffness and cerebrovascular dysfunction in mice correlate with cognitive impairment but are not reduced with long-term ALT-711 treatment.Physiological reports · 2026Article
- Diabetic hyperglycemia-induced glycation regulates tumor vasculature integrity via NF-κB-mediated GM-CSF secretion by tumor cells.Cell biomaterials · 2025Article
- The incidence of coronary in-stent restenosis and the rate of reaching the standard of low-density lipoprotein cholesterol in patients with type 2 diabetes mellitus and unstable angina pectoris treated with ezetimibe and rosuvastatin.Frontiers in cardiovascular medicine · 2025Article
- Cardiometabolic Changes in Sirtuin1-Heterozygous Mice on High-Fat Diet and Melatonin Supplementation.International journal of molecular sciences · 2024Article
- AGTR1rs5186 Polymorphism Is Associated with the Risk of Restenosis after Percutaneous Coronary Intervention: A Meta-Analysis.Journal of cardiovascular development and disease · 2022Review
- Alagebrium and Complications of Diabetes Mellitus.The Eurasian journal of medicine · 2019Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Mechanisms of restenosis in type 2 diabetes mellitus (T2DM) are incompletely elucidated, but advanced glycation end-product (AGE)-induced vascular remodeling likely contributes. We tested the hypothesis that AGE-related collagen cross-linking (ARCC) leads to increased downstream vascular resistance and altered in-stent hemodynamics, thereby promoting neointimal hyperplasia (NH) in T2DM. We proposed that decreasing ARCC with ALT-711 (Alagebrium) would mitigate this response. Abdominal aortic stents were implanted in Zucker lean (ZL), obese (ZO), and diabetic (ZD) rats. Blood flow, vessel diameter, and wall shear stress (WSS) were calculated after 21 days, and NH was quantified. Arterial segments (aorta, carotid, iliac, femoral, and arterioles) were harvested to detect ARCC and protein expression, including transforming growth factor-β (TGF-β) and receptor for AGEs (RAGE). Downstream resistance was elevated (60%), whereas flow and WSS were significantly decreased (44% and 56%) in ZD vs. ZL rats. NH was increased in ZO but not ZD rats. ALT-711 reduced ARCC and resistance (46%) in ZD rats while decreasing NH and producing similar in-stent WSS across groups. No consistent differences in RAGE or TGF-β expression were observed in arterial segments. ALT-711 modified lectin-type oxidized LDL receptor 1 but not RAGE expression by cells on decellularized matrices. In conclusion, ALT-711 decreased ARCC, increased in-stent flow rate, and reduced NH in ZO and ZD rats through RAGE-independent pathways. The study supports an important role for AGE-induced remodeling within and downstream of stent implantation to promote enhanced NH in T2DM.
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