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ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2026

TRIM69 alleviates ultraviolet B irradiation-induced ferroptosis by regulating p53 in human lens epithelial cells.

Yang Sun, Maierdanjiang Ainiwaer, Binghe Xiao, Yingying Hong, Li Ning, Yinghong Ji

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Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Yang Sun *Eye Institute, Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Maierdanjiang Ainiwaer *Eye Institute, Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Binghe Xiao *Eye Institute, Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Yingying HongEye Institute, Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Li NingEye Institute, Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Yinghong JiEye Institute, Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China. jiyh_eent@163.com.ORCID http://orcid.org/0000-0003-3340-5373

Funding

National Natural Science Foundation of China 82070942
6 · The paper itself

Abstract

purposeAge-related cataract (ARC) is the leading cause of visual impairment worldwide, with ultraviolet B (UVB) radiation recognized as a major risk factor. This study aimed to investigate whether UVB induces ferroptosis in human lens epithelial cells (HLECs) and to explore the role of TRIM69 in modulating this process through the p53 signaling pathway.

methodsHLECs were exposed to UVB irradiation, and ferroptosis was assessed by measuring cell viability, reactive oxygen species (ROS) accumulation, glutathione peroxidase 4 (GPX4) expression, and glutathione (GSH) levels. Ferroptosis inhibition was examined using ferrostatin-1 (Fer-1). TRIM69 expression was modulated by overexpression and knockdown, while the interaction with p53 signaling was evaluated through p53 overexpression assays. Western blotting was performed to analyze GPX4 and SLC7A11 expression.

resultsUVB exposure induced ferroptosis in HLECs, evidenced by reduced GPX4 and GSH, elevated ROS, and decreased viability. Fer-1 treatment significantly improved cell viability and suppressed ROS accumulation. TRIM69 overexpression significantly mitigated the effects of UVB irradiation on cell viability, GSH levels and ROS production, whereas knocking down TRIM69 expression exacerbated these effects. Importantly, p53 overexpression reversed the protective effects of TRIM69 and downregulated GPX4 and SLC7A11, implicating p53-dependent signaling in ferroptosis regulation.

conclusionThese findings demonstrate that TRIM69 protects HLECs against UVB-induced ferroptosis by inhibiting p53-mediated suppression of GPX4 and SLC7A11. TRIM69 may represent a promising therapeutic target for preventing oxidative damage and delaying the onset of ARC.

Indexed as

Epithelial CellsFerroptosisGene Expression RegulationLens, CrystallineTripartite Motif ProteinsTumor Suppressor Protein p53Ubiquitin-Protein LigasesUltraviolet RaysBlotting, WesternCataractCells, CulturedCell SurvivalGlutathioneHumansReactive Oxygen SpeciesSignal TransductionGlutathioneReactive Oxygen SpeciesTP53 protein, humanTripartite Motif ProteinsTumor Suppressor Protein p53Ubiquitin-Protein LigasesAge-related cataractFerroptosisP53TRIM69Ultraviolet B

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.