Glaucoma Research Center, Wills Eye Hospital, Philadelphia, Pennsylvania, USA; Department of Ophthalmology, Tanta Medical School, Tanta University, Tanta, Gharbia, Egypt.
Glaucoma Research Center, Wills Eye Hospital, Philadelphia, Pennsylvania, USA; Yale University School of Medicine, New Haven, Connecticut, USA.
Surv Ophthalmol. 2022 Jul-Aug;67(4):1062-1080. doi: 10.1016/j.survophthal.2021.12.003. Epub 2021 Dec 8.
Glaucoma, a progressive optic neuropathy characterized by retinal ganglion cell degeneration and visual field loss, is the leading cause of irreversible blindness worldwide. Intraocular pressure (IOP) is presently the only modifiable risk factor demonstrated to slow or halt disease progression; however, glaucomatous damage persists in almost 50% of patients despite significant IOP reduction. Many studies have investigated the non-IOP-related risk factors that contribute to glaucoma progression as well as interventions that can prevent or delay glaucomatous neurodegeneration and preserve vision throughout life, independently of IOP. A vast number of experimental studies have reported effective neuroprotection in glaucoma, and clinical studies are ongoing attempting to provide strong evidence of effectiveness of these interventions. We look into the current understanding of the pathophysiology of glaucoma and explore the recent advances in non-IOP related strategies for neuroprotection and neuroregeneration in glaucoma.
青光眼是一种进行性视神经病变,其特征为视网膜神经节细胞变性和视野丧失,是全球范围内导致不可逆性失明的主要原因。目前眼压(IOP)是唯一被证实可以减缓或阻止疾病进展的可调节危险因素;然而,尽管眼压显著降低,仍有近 50%的患者存在青光眼损害。许多研究已经探讨了与眼压无关的促进青光眼进展的风险因素,以及可以预防或延迟青光眼性神经退行性变并在整个生命周期内保持视力的干预措施,而不依赖于眼压。大量的实验研究报告了青光眼的有效神经保护作用,并且正在进行临床试验,试图提供这些干预措施有效性的有力证据。我们研究了青光眼的病理生理学的现有认识,并探讨了与眼压无关的神经保护和青光眼神经再生的最新策略。