# Fullerenol Eye Drops Mitigate UVB-Induced Cataract Progression by Inhibiting Oxidative Stress and Cellular Senescence

**Authors:** Lele Zhang, Shuying Chen, Zihao Yu, Yuting Su, Jingyu Zhao, Lanlan Hu, Jinglong Tang, Mingliang Zhang

PMC · DOI: 10.3390/antiox15010118 · Antioxidants · 2026-01-16

## TL;DR

Fullerenol eye drops may delay cataract progression by reducing oxidative stress and cellular aging in mice and human cells.

## Contribution

Fullerenol is shown as a novel nanomedicine for cataract management through inhibiting oxidative stress and senescence.

## Key findings

- Fullerenol preserved lens transparency and structure in UVB-induced mouse cataract models.
- Fullerenol reduced oxidative stress and DNA damage while restoring mitochondrial function in human lens epithelial cells.
- Fullerenol modulated oxidative stress and senescence pathways like MAPK and TGF-β, and downregulated p53–CDKN1A.

## Abstract

Cataracts remain the leading cause of blindness worldwide, and surgery is currently the only effective clinical treatment, as no pharmacological therapy has yet been validated. Here, we explore Fullerenol, a hydroxylated fullerene derivative formulated as eye drops, as a potential nanomedicine for delaying cataract onset and progression. In UVB-induced mouse cataract models, topical Fullerenol preserved the lens transparency and histological structure. In human lens epithelial cells, Fullerenol reduced the oxidative stress, restored the mitochondrial function, alleviated the DNA damage, and suppressed the cellular senescence. RNA sequencing and pathway enrichment analyses further indicated that Fullerenol modulated the oxidative stress- and senescence-associated signaling pathways, including MAPK and TGF-β cascades, while downregulating the p53–CDKN1A (p21) axis. These findings provide new evidence that Fullerenol can mitigate photo-oxidative damage and age-related cellular dysfunction, highlighting its promise as a non-invasive and clinically translatable nanomedicine strategy for cataract management.

## Linked entities

- **Genes:** TP53 (tumor protein p53) [NCBI Gene 7157], CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026]
- **Diseases:** cataract (MONDO:0005129)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026] {aka CAP20, CDKN1, CIP1, MDA-6, P21, SDI1}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}
- **Diseases:** blindness (MESH:D001766), Cataracts (MESH:D002386)
- **Chemicals:** hydroxylated fullerene (-), Fullerenol (MESH:C108127)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12838378/full.md

## References

60 references — full list in the complete paper: https://tomesphere.com/paper/PMC12838378/full.md

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Source: https://tomesphere.com/paper/PMC12838378