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THE INTRINSIC DURABILITY OF AORTIC VALVE ECM IN ABSENCE OF CELLULAR MAINTENANCE

机译:无细胞维持不存在主动脉瓣ECM的内在耐久性

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Without cellular maintenance, AV leaflet fiber network became unfolded, stretched out. and thinned during simulated function for up to 4 weeks. We found that elastin fibers were absence in the flow loop exercised leaflets (Fig. 3). Note that elastin fibers were preserved in the static control that subjected to the same solution environment. Tt could be concluded that degradation along can not explain the absence of elastin in fatigued leaflets. We speculated that mechanical factors caused the loss of elastin fibers that lack of stabilizing crosslinks. The loss of elastin likely accelerated unfolding and straightening of collagen fibers. Mechanically, the structural alteration changed the reference status of fatigued tissue and resulted in a lower net tissue extensibility. We conclude that, in absence of cellular maintenance, decellularized valve leaflets experience rapid structural deterioration due to lack of exogenous stabilizing crosslinks and the structural disruption ss irreversible and cumulative. Apparently, recellularization is a key for the successful development of TEHV via decellularization approach.
机译:没有蜂窝维护,AV传单光纤网络变得展开,伸展出来。在模拟功能期间稀释,最长可达4周。我们发现弹性蛋白纤维在流动回路锻炼叶片中不存在(图3)。注意,在经过相同的溶液环境的静态控制中保留了弹性蛋白纤维。可以得出结论,降解不能解释疲劳传单中的缺乏弹性蛋白。我们推测机械因素导致缺乏稳定交联的弹性蛋白纤维的丧失。弹性蛋白的丧失可能会加速胶原纤维的展开和矫直。机械地,结构改变改变了疲劳组织的参考状态,导致净组织可伸展性较低。我们得出结论,在没有细胞维持的情况下,由于缺乏外源稳定的交联和结构破坏SS而不可逆转和累积,脱细胞化瓣膜叶片由于缺乏外源稳定性和累积而经历了快速的结构性恶化。显然,通过脱细胞化方法是成功发展Tehv的关键。

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