Diet-induced obesity drives negative mouse vein graft wall remodeling.

摘要: Introduction The heightened inflammatory phenotype associated with obesity has been linked to the development of cardiovascular diseases. Short-term high-fat feeding induces a proinflammatory state that may impact blood vessel wall. CD11c, significantly increased dendritic cell biomarker during diet-induced (DIO), have mechanistic role in this effect. We hypothesized effect short-term DIO accelerates vein bypass graft failure via CD11c-dependent mechanisms. Methods Male 9-week-old mice (n = 13, C57BL/6J recipients; n = 6, CD11c -/- recipients) and normal chow controls 15, underwent unilateral carotid interposition isografting (inferior vena cava from same diet genetic background donor), midgraft or outflow focal stenosis. Vein grafts were harvested at either 1 week (immunohistochemical staining for early expression) 4 weeks later (morphometric analyses evaluation). Results Despite 40% larger body size, had 44% smaller poststenosis lumens ( P  = .03) than their an acceleration overall negative wall remodeling day-28 stenosis model but not model. Higher expression occurred midgraft-stenosis walls, both postoperative days 7 28. In contrast, in vivo deficiency, did elicit poststenotic attenuated intimal hyperplasia. Conclusions These findings highlight as potential factor leading provide direct evidence dietary alterations mammalian metabolic milieu can lasting implications related acute vascular interventions. mouse CD11c-depedent pathways.