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Open Access Clinical Research Issue
Effectiveness and safety of superselective ophthalmic artery thrombolysis beyond 24h in central retinal artery occlusion
International Journal of Ophthalmology 2026, 19(4): 720-732
Published: 18 April 2026
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AIM

To evaluate the effectiveness and safety of superselective ophthalmic artery thrombolysis (SOAT) for central retinal artery occlusion (CRAO) beyond 24h after onset.

METHODS

This was a retrospective cohort study of CRAO patients treated from January 2019 to July 2025. Patients were divided into four groups by treatment (SOAT/conservative) and onset-to-treatment time (<24h/>24h). Main outcome measures were best-corrected visual acuity (BCVA, logMAR) and central macular thickness (CMT) assessed via spectral-domain optical coherence tomography (SD-OCT), recorded at baseline, 3d and 1mo after treatment. Ocular/systemic adverse events were documented.

RESULTS

A total of 109 CRAO participants were enrolled, including 74 males (67.89%) and 35 females (32.11%), with a mean age of 52.30±11.76y. Underlying diseases were hypertension (78 cases, 71.56%), diabetes (40 cases, 36.70%), arterial atherosclerosis with plaque formation (81 cases, 74.31%), hyperlipidemia (14 cases, 12.84%), and hypercholesterolemia (16 cases, 14.68%). Four groups included 25, 28, 26, and 30 cases in Groups 1 (SOAT<24h), 2 (SOAT>24h), 3 (conservative <24h), and 4 (conservative >24h), respectively. In <24h cohort, BCVA improved significantly in both Group 1 (2.36±0.53 to 1.71±0.81 logMAR, P<0.05) and Group 3 (2.42±0.40 to 1.92±0.76 logMAR, P<0.05). In >24h cohort, thrombolysis improved BCVA (1.84±0.88 to 1.31±0.53 logMAR, P<0.05), while conservative treatment showed no significant change (2.04±0.74 to 1.92±0.73 logMAR, P=0.808). Clinically significant improvement (≥0.3 logMAR) was more frequent with SOAT in both time windows (P<0.05). SOAT significantly reduced CMT in both <24h (256±25.65 to 209±21.22 μm, P<0.001) and >24h groups (242±23.33 to 204±27.22 μm, P<0.001), while conservative treatment had no significant effect on CMT (all P>0.05). Adverse events included orbital swelling (11.3%), new cerebral infarction (7.55%), dizziness/headache (7.55%), and nausea/vomiting (5.66%). No intracranial hemorrhage occurred.

CONCLUSION

SOAT provides meaningful visual and anatomical benefit even beyond 24h after symptom onset. However, potential ocular and systemic adverse events necessitate careful patient selection and individualized risk assessment.

Open Access Basic Research Issue
Nintedanib regulates miR-23b-3p/TGFBR2 axis and competitively binds to TGFBR2 protein, inhibiting EMT process in human pterygium cells
International Journal of Ophthalmology 2025, 18(5): 779-791
Published: 18 May 2025
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AIM

To investigate the effects of nintedanib on epithelial-mesenchymal transition (EMT) in cells derived from pterygium, aiming to explore its potential as a pharmacological intervention for pterygium treatment.

METHODS

Primary human pterygium epithelial cells (hPEC) and human conjunctival epithelial (hCJE) cells were isolated from patients, cultured, and characterized. The impact of nintedanib on transforming growth factor beta (TGF-β)-induced EMT was assessed by examining the expression of EMT markers such as vimentin and E-cadherin. Additionally, the modulation of the miR-23b-3p/transforming growth factor beta receptor 2 (TGFBR2)/Smad2 pathway by nintedanib was investigated to elucidate its potential antifibrotic mechanism.

RESULTS

The expression of miR-23b-3p gene in hCJE cells was significantly higher than that in hPEC cells. Nintedanib effectively mitigated TGF-β-induced EMT in cells derived from pterygium, as evidenced by the downregulation of vimentin and upregulation of E-cadherin. When the nintedanib concentration exceeded 1 μmol/L, it significantly suppressed the proliferation of hPEC cells and significantly inhibited the migration distance of hPEC cells within 48h (P<0.01). The immunoprecipitation experiment showed that nintedanib modulated the TGFBR2 protein’s response to TGF-β independently of miR-23b-3p. Both nintedanib and transfection with miR-23b-3p mimic significantly inhibited the expression levels of phosphorylated Smad2, snail homolog 1 (Drosophila, SNAIL), and SNAI2 (also known as SLUG, snail family transcriptional repressor 2) proteins.

CONCLUSION

Nintedanib is found to modulate the miR-23b-3p/TGFBR2/Smad2 pathway, suggesting a novel antifibrotic mechanism. These findings collectively highlight nintedanib’s therapeutic potential in managing pterygium, marking a significant step toward non-surgical treatment options. Nintedanib may offer a targeted pharmacological treatment that could complement or reduce the need for surgical interventions.

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