【摘要】 内膜增生（IH）是多种血管疾病的共同病理特征，特别是在动脉粥样硬化、支架内再狭窄（ISR）以及自体动静脉内瘘（AVF）功能障碍等过程中，均可观察到显著的IH。近年来，内皮细胞（ECs）在IH中的作用受到越来越多的关注。ECs不仅是血管壁的重要组成部分，还在血管稳态维持、炎症调节、血管重塑进程中发挥关键作用。文章系统综述有关ECs在IH中角色的近期研究进展，重点探讨ECs在血管损伤后引发IH的各类机制，包括内皮屏障功能与分泌功能的障碍、内皮-间充质转化（EndMT）以及炎症激活与调控。深入理解ECs在IH发生与发展中的作用机制，将为针对ECs损伤引发的血管疾病的防治策略提供新的思路和潜在的治疗靶点。更多还原

【Abstract】 Intimal hyperplasia(IH) emerges as a unifying pathological hallmark across diverse vasculopathic conditions, with pronounced manifestations notably implicated in atherosclerosis, in-stent restenosis(ISR), and dysfunction of autogenous arteriovenous fistulas(AVFs). Recent years have witnessed growing attention to the mechanistic contributions of endothelial cells(ECs) to IH pathogenesis. ECs, as integral components of the vascular wall, play pivotal roles in maintaining vascular homeostasis, modulating inflammatory responses, and orchestrating vascular remodeling processes. This article systematically reviews recent advancements in understanding the roles of ECs in IH, with a focused exploration of the multifaceted mechanisms through which ECs contribute to IH pathogenesis following vascular injury. Key mechanisms include compromised endothelial barrier and secretory functions, endothelialmesenchymal transition(EndMT), and the activation and regulation of inflammatory pathways. Elucidating these EC-driven mechanisms underlying IH initiation and progression may unveil novel therapeutic strategies and potential molecular targets for managing vasculopathies arising from EC dysfunction.更多还原