缺氧作为一种关键的病理生理刺激因素，在血管疾病尤其是自体动静脉内瘘(arteriovenous fistula，AVF)功能障碍的发生发展中扮演着重要角色。血管平滑肌细胞(vascular smooth muscle cells，VSMCs)的表型转换是血管重塑及病理变化的核心机制，缺氧环境显著影响其从收缩型向合成型的转变，进而促进血管壁重构和内膜增生，导致AVF通畅性受损。尽管近年来对缺氧诱导的VSMCs表型转换机制已有较多研究，但其分子调控网络复杂，尚存在诸多待解问题。本文系统综述了缺氧条件下VSMCs表型转换的分子机制，涵盖关键信号通路、转录因子及表观遗传调控机制，并分析其在AVF功能障碍中的具体作用及相关潜在治疗靶点。旨在为深入理解AVF病理机制及开发有效干预策略提供理论支持和研究方向，促进AVF的长期稳定功能。

Hypoxia is a critical pathophysiological stimulus and plays a pivotal role in the pathogenesis and progression of vascular diseases, particularly in the dysfunction of autologous arteriovenous fistula (AVF). The hypoxia-induced phenotypic switch of vascular smooth muscle cells (VSMCs) is a key step leading to vascular remodeling and other pathological alterations. Hypoxia promotes the transition of VSMCs from a contractile phenotype to a synthetic phenotype, resulting in vascular wall reconstruction, neointimal hyperplasia and ultimately compromised AVF patency. Although considerable researches on hypoxia-induced VSMCs phenotypic switch have been conducted in recent years, its molecular regulatory network remains intricate with many unresolved problems. This article systematically reviews molecular mechanism of VSMCs phenotypic switch under hypoxia, encompassing key signaling pathways, transcription factors and epigenetic regulatory features, and emphasizes their specific roles in AVF dysfunction and potential therapeutic targets, in order to provide theoretical support and research directions for better comprehension  of AVF pathology and for design of effective intervention strategies to maintain long-term and stable function of AVFs.