Chapter 34: Hyperosmotics

Han Xue, Zhu Zhaoqi, Song Ziyue et al.

UGX-201 optogenetic therapy for advanced RP was safe and well-tolerated. It restored light perception in some and improved vision in others, showing potential as a mutation-independent treatment.

Gao, Zhaolin, Yu, Haiyang, Duan, Tianqi et al.

This study found activating AMPK reduces retinal ganglion cell apoptosis in experimental glaucoma models by inhibiting mTOR, suggesting AMPK is a potential therapeutic target for glaucoma.

Zhang Jiali, Chen Xinyi, Ji Jing et al.

Activating or overexpressing TASK-3 potassium channels protected retinal ganglion cells and restored vision in mice with optic nerve injury, suggesting a novel therapeutic strategy for RGC degeneration.

Hai-Chao Chen, Fu-Lin Gao, Jia-Xin Cao et al.

Studying mouse models, retinal pericyte loss worsens Alzheimer's-related amyloid and tau pathology, impairs ocular waste clearance, and damages retinal structure, highlighting pericytes as a therapeutic target.

Wirostko Barbara M, Roy Chowdhury Uttio, Brandano Lisa A et al.

QLS-111, a novel potassium channel opener, safely and effectively lowered eye pressure in animals, showing additive benefits with existing glaucoma drugs by reducing episcleral venous pressure, promising a new treatment.

Bala Suraj, Allan Kevin C, Decker Nicole L et al.

GLP-1RAs' ophthalmic effects are inconsistent, showing conflicting impacts on retinopathy/optic neuropathy but potential protection for glaucoma, dry eye, and IIH. More robust studies are needed.

Xia Fan, Shi Shuizhen, Palacios Erick et al.

This study found that blocking CXCR3 signaling, which mediates astrocyte-RGC communication via C3/C3aR, prevented retinal ganglion cell loss in a mouse glaucoma model. This offers a promising IOP-independent therapeutic target.

Loughman James, Lingham Gareth, Kaymak Hakan et al.

MyopiaX, a blue-light smartphone app, was studied for juvenile myopia control. It was safe and well-tolerated, but showed no significant benefit over DIMS spectacles in slowing myopia progression.

Ruzafa Noelia, Pereiro Xandra, Prieto-López Laura et al.

This study found that in glaucoma, CART-positive RGCs are highly vulnerable, while OPN4-positive RGCs (ipRGCs) are more resistant, suggesting targeted neuroprotection for specific RGC subtypes.

Young Su Ling, Gazzard Gus

This review found oral niacin/nicotinamide cause diverse, dose-dependent side effects (e.g., GI upset, flushing), with nicotinamide generally safer. Clinicians should be aware of these AEs, especially for glaucoma patients using these supplements.

Baez Hector C, LaPorta Jennifer M, Walker Amber D et al.

Researchers showed that peeling the inner limiting membrane before gene therapy injection expands retinal ganglion cell calcium imaging beyond the fovea. This enables broader study of retinal function and potential gene therapies.

Chen Meini, Zhang Xuan, Zeng Zhou et al.

Resveratrol protected retinal cells from IR injury by inhibiting inflammation and cell death via the Bcl3/NF-κB p50 pathway. This identifies a novel neuroprotective target for glaucoma.

Qiu ChunTing, Zhang Ting, Wang Qin et al.

This study found Connexin 36 gap junctions mediate retinal ganglion cell death after corneal alkali burns. Blocking Cx36 with a drug (MFA) or genetic knockout protected these cells, suggesting a neuroprotective therapeutic target.

Gao Jia, Wang Wei, Mo Ya

This review highlights that complement system activation and microglial crosstalk create a damaging positive feedback loop in retinal degenerative diseases like glaucoma, suggesting these pathways are therapeutic targets.

Takahashi Naoki, Tawarayama Hiroshi, Chida Yuri et al.

ENO1 dysfunction impairs glycolysis, making RGCs overly dependent on OXPHOS for energy under stress, which worsens RGC death. Preventing this glycolytic attenuation could be a glaucoma treatment.

Sheng Yifei, Yang Xiaojing, Qiu Jianfeng et al.

MRI showed POAG patients have impaired brain glymphatic function (larger choroid plexus, weaker CSF clearance), suggesting this neurodegenerative process contributes to glaucoma pathophysiology.

Ye Huiwen, Feng Yanlin, Xiang Wu et al.

Ferroptosis contributes to retinal ganglion cell loss in a normal tension glaucoma model. Inhibiting ferroptosis protected RGCs and visual function, suggesting a promising NTG therapeutic strategy.

Tan Jit Kai, Steel David H, Ahmad Sajjad et al.

ROCK inhibitors are safe and effective for glaucoma by lowering IOP, and show promise for corneal and retinal diseases by improving cell function and reducing inflammation.