表面改性在缓解氧化应激引起的瓣膜退化方面取得进展

Q1 Engineering
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引用次数: 0

摘要

瓣膜性心脏病(VHD)是一种严重威胁公众健康的疾病,心脏瓣膜置换手术是治疗严重病例的标准方法。尽管人工心脏瓣膜技术不断进步,但由于体内退化,其寿命仍然有限。因此,迫切需要有效的方法来提高人工心脏瓣膜的耐用性。由于氧化应激(OS)是导致心血管植入物失效的一个关键驱动因素,本综述将重点探讨氧化应激如何在心脏瓣膜退化中发挥关键作用,以及它与细胞外基质(ECM)降解、免疫反应、血栓形成和脂质代谢这四大生理机制之间的关系。通过强调OS是潜在的治疗靶点,我们探讨了结合这些基本机制的表面修饰策略,包括消除OS、免疫抑制、阻断表面降解活性基团和抗凝等被动方法,以及调节生物功能恢复和表面内皮重塑等主动方法。这些策略旨在结合OS调节的观点,延缓或逆转人工瓣膜的退化,最终延长心脏瓣膜置换手术后的预后期。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Advances of surface modification to alleviate oxidative stress-induced valve degeneration

Advances of surface modification to alleviate oxidative stress-induced valve degeneration

Valvular heart disease (VHD) is a significant public health threat, with heart valve replacement surgery being the standard treatment for severe cases. Despite of advancements in artificial heart valves, their longevity remains limited due to in vivo degeneration. In consequence, there is an urgent need for effective methods to enhance the durability of artificial heart valves. Because oxidative stress (OS) is a key driving factor contributing to the failure of cardiovascular implants, this review focuses on how OS plays a critical role in heart valve degeneration, and its relationship with four major physiological mechanisms: extracellular matrix (ECM) degradation, immune response, thrombosis and lipid metabolism. By highlighting OS as a potential therapeutic target, we explore surface modification strategies that incorporate these fundamental mechanisms, refer to passive approaches including OS elimination, immunosuppression, blocking surface-degradation active groups, and anticoagulation, and active approaches such as regulating biological function recovery, and surface endothelial remodeling. These strategies aim to delay or reverse artificial valves degeneration via combining with the perspective of OS regulation, ultimately extending the prognosis period after heart valve replacement surgeries.

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来源期刊
Smart Materials in Medicine
Smart Materials in Medicine Engineering-Biomedical Engineering
CiteScore
14.00
自引率
0.00%
发文量
41
审稿时长
48 days
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