Hypoxic eye diseases represent a pivotal yet often underappreciated contributor to the onset and progression of many retinal disorders. When hypoxia persists or exceeds the tissue’s compensatory capacity, it triggers pathological retinal neovascularization, blood–retinal barrier disruption, and neuronal apoptosis, ultimately resulting in irreversible visual impairment. Connexins (Cxs) form gap junction channels and hemichannels and regulate retinal cell proliferation, differentiation, and survival, thereby playing a central regulatory role in the pathogenesis of hypoxic ocular diseases. In addition to gap junctions, Cx hemichannels promote transmission of molecules between intra- and extracellular environments, further influencing retinal homeostasis under hypoxic stress. This review synthesizes recent progress in understanding connexins in localized and systemic hypoxic eye diseases. We focus on the molecular mechanisms underlying the development and progression of hypoxia-induced ocular pathology, with particular emphasis on the emerging potential of Cxs as novel therapeutic targets for hypoxic ocular diseases. Following a systematic literature search, the electronic databases PubMed and EMBASE were consulted, with the search deadline set at December 2025. The search terms employed were as follows: hypoxia, connexin, gap junctions, hemichannels.
Zhang et al. (2026) studied this question.