Yang Yuchen, Zou Haidong
Shanghai Eye Diseases Prevention & Treatment Center/Shanghai Eye Hospital, School of Medicine, Tongji University, Shanghai, China.
Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Front Endocrinol (Lausanne). 2025 May 21;16:1587231. doi: 10.3389/fendo.2025.1587231. eCollection 2025.
Diabetic retinopathy (DR) is a primary cause of vision loss among individuals with diabetes and represents the most prevalent microvascular complication of diabetes mellitus. Its pathophysiological mechanisms involve processes such as oxidative stress, chronic inflammation, cell apoptosis, and angiogenesis. As a core transcription factor in the antioxidant response, Nrf2 upregulates the expression of antioxidant genes through the Keap1-Nrf2-ARE pathway, hence reducing reactive oxygen species (ROS) levels in retinal cells and alleviating oxidative stress and correlated damage. By activating Nrf2, the release of pro-inflammatory cytokines is inhibited, which helps mitigate inflammation and delays DR progression through anti-apoptotic effects, suppression of angiogenesis and ferroptosis inhibition. This review highlights the Nrf2-related regulatory mechanisms and the latest research progress regarding its function in DR, offering a theoretical foundation for Nrf2-targeted DR therapies.
糖尿病视网膜病变（DR）是糖尿病患者视力丧失的主要原因，也是糖尿病最常见的微血管并发症。其病理生理机制涉及氧化应激、慢性炎症、细胞凋亡和血管生成等过程。作为抗氧化反应中的核心转录因子，Nrf2通过Keap1-Nrf2-ARE途径上调抗氧化基因的表达，从而降低视网膜细胞中的活性氧（ROS）水平，减轻氧化应激及相关损伤。通过激活Nrf2，可抑制促炎细胞因子的释放，这有助于减轻炎症，并通过抗凋亡作用、抑制血管生成和抑制铁死亡来延缓DR的进展。本文综述强调了Nrf2相关的调控机制及其在DR中的功能的最新研究进展，为针对Nrf2的DR治疗提供理论基础。
