Suture exposure remains to be a potential problem of transscleral fixated posterior chamber intraocular lens (PCIOL). We report a modified technique to minimize the risk of suture exposure for the transscleral fixation of PCIOL. The modified surgical technique is as following: at first, two 3 mm × 4 mm square scleral pockets were created from groove incisions at opposite positions. A straight needle attached to a 10–0 polypropylene suture was passed through one incision groove. Then, a 27-Gauge hollow needle passed through the opposite sclera incision bed was used to retrieve the straight fine needle via its barrel. The sutures were tied to themselves after one more bite on the scleral bed. At last, the suture ends were left long (about 4 mm) and laid flat into corresponding laminar scleral pockets. This modified technique of PCIOL was performed in 48 post-traumatic aphakic vitrectomized eyes from 48 patients (47 male, one female) with mean age of 34.8 ± 14.8 years. Main outcome measures included best corrective visual acuity (BCVA), IOL decentration, IOL tilt, and postoperative complications. The mean follow-up was 32.3 ± 10.8 months (3–67 months). The LogMAR BCVA remained stable, from a preoperative value of 0.46 ± 0.34 to postoperative 0.44 ± 0.34 (p = 0.69). Mild IOL tilt (5–10°) was observed in five eyes, and slight IOL decentration (0.5–1.0 mm) was seen in three cases. No case of suture exposure, suture breakage, IOL dislocation, or endophthalmitis was observed during the follow up period. The modified technique allowed stable placement of PCIOLs in post-traumatic aphakic eyes with a wide range of follow-up. Our procedure might have the potential benefit to avoid suture exposure in scleral-fixated IOL implantation.

Purpose: This study aimed to explore the impact of GSK840 on retinal neuronal injury after retinal ischemia/reperfusion (IR) and its associated mechanism. Methods: We established an in vivo mouse model of IR and an in vitro model of oxygen and glucose deprivation/reoxygenation (OGDR) in primary mouse retinal ganglion cells (RGCs). GSK840, a small-molecule compound, was used to specifically inhibit RIPK3/MLKL-dependent necroptosis. Retinal structure and function evaluation was performed by using hematoxylin and eosin staining, optical coherence tomography, and electroretinography. Propidium Iodide (PI) staining was used for detection of necroptotic cell death, whereas Western blot analysis and immunofluorescence were used to assess necroptosis-related proteins and inner retinal neurons. Results: RIPK3/MLKL-dependent necroptosis was rapidly activated in RGCs following retinal IR or OGDR. GSK840 helped maintain relatively normal inner retinal structure and thickness by preserving inner retinal neurons, particularly RGCs. Meanwhile, GSK840 ameliorated IR-induced visual dysfunction, as evidenced by the improved amplitudes of photopic negative response, a-wave, b-wave, and oscillatory potentials. And GSK840 treatment significantly reduced the population of PI⁺ RGCs after injury. Mechanistically, GSK840 ameliorated RGC necroptosis by inhibiting the RIPK3/MLKL pathway. Conclusions: GSK840 exerts protective effects against retinal neuronal injury after IR by inhibiting RIPK3/MLKL-mediated RGC necroptosis. GSK840 may represent a protective strategy for RGC degeneration in ischemic retinopathy.

Glaucoma, a prevalent cause of permanent visual impairment worldwide, is characterized by the progressive degeneration of retinal ganglion cells (RGCs). NADPH oxidase (NOX) 1 and NOX4 are pivotal nodes in various retinal diseases. Setanaxib, a potent and highly selective inhibitor of NOX1 and NOX4, can impede the progression of various diseases. This study investigated the efficacy of setanaxib in ameliorating retinal ischemia-reperfusion (I/R) injury and elucidated its underlying mechanisms. The model of retinal I/R induced by acute intraocular hypertension and the oxygen-glucose deprivation/reoxygenation (OGD/R) model of primary RGCs were established. By suppressing NOX1 and NOX4 expression in RGCs, setanaxib mitigated I/R-induced retinal neuronal loss, structural disruption, and dysfunction. Setanaxib reduced TUNEL-positive cells, upregulated Bcl-2, and inhibited Bax, Bad, and cleaved-caspase-3 overexpression after I/R injury in vitro and in vivo. Moreover, setanaxib also significantly reduced cellular senescence, as demonstrated by downregulating SA-β-gal-positive and p16-INK4a expression. Furthermore, setanaxib significantly suppressed ROS production, Hif-1α and FOXO1 upregulation, and NRF2 downregulation in damaged RGCs. These findings highlight that the setanaxib effectively inhibited NOX1 and NOX4, thereby regulating ROS production and redox signal activation. This inhibition further prevents the activation of apoptosis and senescence related factors in RGCs, ultimately protecting them against retinal I/R injury. Consequently, setanaxib exhibits promising potential as a therapeutic intervention for glaucoma.

As part of the central nervous system, the optic nerve, composed of axons from retinal ganglion cells (RGCs), generally fails to regenerate on its own when injured in adult mammals. An innovative approach to promoting optic nerve regeneration involves manipulating the interactions between amacrine cells (ACs) and RGCs. Here, we identified a unique AC subtype, dopaminergic ACs (DACs), that responded early after optic nerve crush by down-regulating neuronal activity and reducing retinal dopamine (DA) release. Activating DACs or augmenting DA release with levodopa demonstrated neuroprotective effects and modestly enhanced axon regeneration. Within this context, we pinpointed the DA receptor D1 (DRD1) as a critical mediator of DAC-derived DA and showed that RGC-specific Drd1 overexpression effectively overcame subtype-specific barriers to regeneration. This strategy markedly boosted RGC survival and axon regeneration after crush and preserved vision in a glaucoma model. This study unveils the crucial role of DAC-derived DA signaling in optic nerve regeneration, holding promise for therapeutic insights into neural repair.

Reactive oxygen species (ROS) overproduction plays an essential role in the etiology of ischemic/hypoxic retinopathy caused by acute glaucoma. NADPH oxidase (NOX) 4 was discovered as one of the main sources of ROS in glaucoma. However, the role and potential mechanisms of NOX4 in acute glaucoma have not been fully elucidated. Therefore, the current study aims to investigate the NOX4 inhibitor GLX351322 that targets NOX4 inhibition in acute ocular hypertension (AOH)-induced retinal ischemia/hypoxia injury in mice. Herein, NOX4 was highly expressed in AOH retinas, particularly the retinal ganglion cell layer (GCL). Importantly, the NOX4 inhibitor GLX351322 reduced ROS overproduction, inhibited inflammatory factor release, suppressed glial cell activation and hyperplasia, inhibited leukocyte infiltration, reduced retinal cell senescence and apoptosis in damaged areas, reduced retinal degeneration and improved retinal function. This neuroprotective effect is at least partially associated with mediated redox-sensitive factor (HIF-1α, NF-κB, and MAPKs) pathways by NOX4-derived ROS overproduction. These results suggest that inhibition of NOX4 with GLX351322 attenuated AOH-induced retinal inflammation, cellular senescence, and apoptosis by inhibiting the activation of the redox-sensitive factor pathway mediated by ROS overproduction, thereby protecting retinal structure and function. Targeted inhibition of NOX4 is expected to be a new idea in the treatment of acute glaucoma.

To investigate the anatomic and functional outcomes of pars plana vitrectomy (PPV) with partial tamponade of filtered air for rhegmatogenous retinal detachment (RRD) caused by superior retinal breaks. Retrospective, comparative, consecutive case series study. Patients with RRD caused by superior retinal breaks undergone PPV with partial tamponade (Group A) and whole tamponade (Group B) of filtered air were included. The main outcomes were primary and final success rates, best corrected visual acuity (BCVA), and rate of postoperative cataract surgery. Forty-one patients (41 eyes) were included in Group A and 36 patients (36 eyes) were included in Group B. There were no significant differences in primary or final success rates between Groups A and B (P = 0.618 and P = 1.000, respectively). The patients in Group A experienced quicker postoperative vision improvement (from the Week 1 follow-up) than the patients in Group B (from the Month 3 follow-up). The postoperative cataract surgery rate of Group A (7/31) was lower than that of Group B (13/26) (P = 0.031). PPV with partial tamponade of air is effective in achieving a high anatomic success rate, quicker postoperative vision improvement, and lower rate of postoperative cataract surgery in RRD caused by superior retinal breaks.