@article{Xu2026, 
author = {Jing Xu and Mei Sun and Chen Wang and Pin Ju and Xiao-Duo Guan and Li-Ke Xie and Xiao-Feng Hao},
title = {Ferroptosis and microglial polarization in retinal vein occlusion: pathological mechanisms and therapeutic strategies},
year = {2026},
journal = {International Journal of Ophthalmology},
volume = {19},
number = {4},
pages = {808-814},
keywords = {ferroptosis, microglial polarization, retinal vein occlusion, iron metabolism dysregulation, lipid peroxidation},
url = {https://www.sciopen.com/article/10.18240/ijo.2026.04.21},
doi = {10.18240/ijo.2026.04.21},
abstract = {With the acceleration of global aging, the incidence of retinal vein occlusion (RVO) has risen markedly. Its pathogenic mechanisms are closely linked to iron dyshomeostasis and microglial polarization and age-related degenerative changes in retinal microvessels. We systematically summarize the regulatory mechanisms of ferroptosis—an iron-dependent, lipid peroxidation-driven form of cell death, and elucidate the central pathway by which iron overload exacerbates retinal injury through the synergy of hypoxia-reoxygenation (H/R). Specifically, iron metabolic imbalance catalyzes the production of reactive oxygen species (ROS) via the Fenton reaction, which drives the polarization of microglia toward the proinflammatory M1 phenotype and activates the acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated lipid peroxidation cascade. This review proposes novel insights for combinatorial therapeutic strategies targeting key ferroptotic pathways (e.g., the SLC7A11/GPX4 axis) and modulating microglial polarization, while also addressing the translational challenges associated with iron chelators (deferoxamine), lipid peroxidation inhibitors (liproxstatin-1), and targeted delivery systems for RVO.}
}