The Journal of surgical research · 2026
Fluvastatin and vascular endothelial growth factor Containing Resins Promote Angiogenesis and Arteriogenesis.
СтатьяНазвание и аннотация: Перевод в очереди
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Maier Kristopher G, Muqri Furqan, Guo Dandan, Kassem Mohammed, DaCosta Mary, Bruch David, Luo Juntao, Gahtan Vivian
Аннотация
INTRODUCTION: Many patients with chronic limb threatening ischemia rely on neovascularization. Statins and vascular endothelial growth factor (VEGF) stimulate neovascularization. We hypothesized that locally delivered TentaGel (TG) resins containing VEGF-165A or fluvastatin would increase neovascularization in hindlimb ischemia and their combination would be most effective.
METHODS: Hydrogel resins were loaded with fluvastatin or VEGF-165A. Endothelial angiogenesis and proliferation were examined with free VEGF-165A, fluvastatin, resin, or resin bound VEGF-165A and/or fluvastatin. In hindlimb ischemia, TG resin-bound VEGF-165A, fluvastatin-bound resin, or a combination were injected into rat hindlimbs. Doppler flow was measured at pre and postoperative days 1, 3, 7 and 14. On day 14, the vastus was stained for arteriogenesis and the gastrocnemius for angiogenesis.
RESULTS: In vitro, hydrogel resins took up VEGF-165A surrogate and fluvastatin. Resins released fluvastatin at 10% per 24 h. Unloaded resin had no effect on endothelial cells (ECs). Both free and resin-bound fluvastatin or VEGF-165A promoted EC proliferation and tubule formation. In vivo, blood flow at day 14 with untreated or empty resin showed partial recovery of blood flow, while TG resin-bound fluvastatin returned flow to preoperative levels. The combination increased flow more than fluvastatin alone, and resin-bound VEGF-165A alone had the greatest increase in flow. Resin-bound fluvastatin, resin-bound VEGF-165A, or both increased angiogenesis and arteriogenesis.
CONCLUSIONS: In vitro, both free and resin-bound fluvastatin and VEGF-165A equally promoted EC proliferation and tubule formation. In vivo, neovascularization and blood flow improved with VEGF-165A or fluvastatin-bound resins. Resin-bound VEGF-165A was strongest in vivo and warrants further study.
METHODS: Hydrogel resins were loaded with fluvastatin or VEGF-165A. Endothelial angiogenesis and proliferation were examined with free VEGF-165A, fluvastatin, resin, or resin bound VEGF-165A and/or fluvastatin. In hindlimb ischemia, TG resin-bound VEGF-165A, fluvastatin-bound resin, or a combination were injected into rat hindlimbs. Doppler flow was measured at pre and postoperative days 1, 3, 7 and 14. On day 14, the vastus was stained for arteriogenesis and the gastrocnemius for angiogenesis.
RESULTS: In vitro, hydrogel resins took up VEGF-165A surrogate and fluvastatin. Resins released fluvastatin at 10% per 24 h. Unloaded resin had no effect on endothelial cells (ECs). Both free and resin-bound fluvastatin or VEGF-165A promoted EC proliferation and tubule formation. In vivo, blood flow at day 14 with untreated or empty resin showed partial recovery of blood flow, while TG resin-bound fluvastatin returned flow to preoperative levels. The combination increased flow more than fluvastatin alone, and resin-bound VEGF-165A alone had the greatest increase in flow. Resin-bound fluvastatin, resin-bound VEGF-165A, or both increased angiogenesis and arteriogenesis.
CONCLUSIONS: In vitro, both free and resin-bound fluvastatin and VEGF-165A equally promoted EC proliferation and tubule formation. In vivo, neovascularization and blood flow improved with VEGF-165A or fluvastatin-bound resins. Resin-bound VEGF-165A was strongest in vivo and warrants further study.