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An APE1 Redox Inhibitor Attenuates Pathological Retinal Vascularization by Suppressing FGF2 Angiogenic Signaling.
Chenfei Yan1, Qiangqiang Fu2, Jiawei Wang1
1Department of Ophthalmology, Qilu Hospital of Shandong University, Jinan, People's Republic of China.
Investigative Ophthalmology & Visual Science
|March 20, 2026
Summary
A new study shows that inhibiting Apurinic/apyrimidinic endonuclease 1 (APE1) with Refi-10 can treat retinal neovascular (RNV) diseases. This approach targets fibroblast growth factor 2 (FGF2) and offers an alternative to anti-VEGF therapies.
Area of Science:
- Ophthalmology
- Molecular Biology
- Pharmacology
Background:
- Retinal neovascular (RNV) diseases cause significant vision loss.
- Current anti-VEGF therapies face resistance and require frequent injections.
- Apurinic/apyrimidinic endonuclease 1 (APE1) is involved in RNV pathogenesis.
Purpose of the Study:
- To evaluate APE1 as a therapeutic target for RNV.
- To assess the efficacy of the APE1 redox inhibitor Refi-10 for vascular retinopathies.
- To elucidate the mechanisms underlying Refi-10's action in RNV.
Main Methods:
- An oxygen-induced retinopathy (OIR) mouse model was used.
- Refi-10's therapeutic efficacy and mechanisms were investigated.
- Transcriptomic analysis and cellular studies in RPE and hRMECs were performed.
Main Results:
- Refi-10 significantly reduced pathological angiogenesis and ameliorated RNV.
- Refi-10 attenuated inflammation and angiogenesis by inhibiting APE1.
- Refi-10 mitigated RNV by suppressing fibroblast growth factor 2 (FGF2) without affecting VEGF.
Conclusions:
- APE1 and FGF2 signaling are promising therapeutic targets for RNV.
- Refi-10 demonstrates potential as a drug candidate for vascular retinopathies.
- Refi-10 offers a complementary or alternative strategy to VEGF inhibition.
