TNF-α functions as a master regulator of inflammation, and it plays a prominent role in several immunological diseases. By promoting important cellular mechanisms, such as cell proliferation, migration, and phenotype switch, TNF-α induces its exacerbating effects, which are the underlying cause of many proliferative diseases such as cancer and cardiovascular disease. TNF-α primarily alters the immune component of the disease, which subsequently affects normal functioning of the cells. Monoclonal antibodies and synthetic drugs that can target TNF-α and impair its effects have been developed and are currently used in the treatment of a few select human diseases. Vascular restenosis is a proliferative disorder that is initiated by immunological mechanisms. In this review, the role of TNF-α in exacerbating restenosis resulting from neointimal hyperplasia, as well as molecular mechanisms and cellular processes affected or induced by TNF-α, are discussed. As TNF-α-targeting drugs are currently not approved for the treatment of restenosis, the summation of the topics discussed here is anticipated to provide information that can emphasize on the use of TNF-α-targeting drug candidates to prevent vascular restenosis.
肿瘤坏死因子-α（TNF-α）是炎症反应的核心调控因子，在多种免疫性疾病中发挥关键作用。通过促进细胞增殖、迁移及表型转换等重要细胞机制，TNF-α可加剧疾病进程，这成为癌症与心血管疾病等增殖性疾病的根本诱因。TNF-α主要通过改变疾病的免疫组分，进而影响细胞的正常功能。目前针对TNF-α的单克隆抗体及合成药物已成功研发，可特异性抑制其生物学效应，并应用于部分人类疾病的临床治疗。血管再狭窄作为一种由免疫机制触发的增殖性疾病，其病理过程与TNF-α密切相关。本综述系统探讨了TNF-α在新生内膜增生所致再狭窄恶化中的作用机制，并详细阐述了TNF-α影响或诱导的分子通路及细胞过程。鉴于目前靶向TNF-α药物尚未获批用于再狭窄治疗，本文通过对现有研究的整合分析，旨在为开发靶向TNF-α的候选药物以预防血管再狭窄提供理论依据。
肿瘤(癌症)患者之家