A novel protein encoded by hsa_circ_0068626 contributes to age-related cataract via the p62/Keap1/Nrf2 signaling pathway-mediated ferroptosis.

Yuxin Chen, Huajian Li, Lei Wu, Xi Zou, Yue Zhang, Rongrong Huang, Yong Wang

Department of Ophthalmology, Southeast University Affiliated Nantong First People's Hospital, Nantong, Jiangsu, China; Department of Ophthalmology, Yangzhou Maternal and Child Health Care Hospital Affiliated to Yangzhou University, Yangzhou, Jiangsu, China; Department of Ophthalmology, The Second Affiliated Hospital of Nantong University and First People's Hospital of Nantong City, Nantong, Jiangsu, China.Department of Ophthalmology, Southeast University Affiliated Nantong First People's Hospital, Nantong, Jiangsu, China; Department of Ophthalmology, Yangzhou Maternal and Child Health Care Hospital Affiliated to Yangzhou University, Yangzhou, Jiangsu, China; Department of Ophthalmology, The Second Affiliated Hospital of Nantong University and First People's Hospital of Nantong City, Nantong, Jiangsu, China. · pubmed

Paper

Abstract

This study investigates whether circular RNAs (circRNAs) modulate ferroptosis in lens epithelial cells (LECs) during age-related cataract (ARC) pathogenesis via novel encoded proteins. Initial circRNA-sequencing identified hsa_circ_0068626 (circTFRC) as significantly upregulated in ARC, predominantly localized to the cytoplasm through nuclear-cytoplasmic fractionation and fluorescence in situ hybridization (FISH). Functional assays revealed that circTFRC depletion impaired LECs proliferation and viability, while overexpression exacerbated ferroptosis, evidenced by elevated intracellular reactive oxygen species (ROS) and Fe

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Research summary

The paper claims that hsa_circ_0068626 contributes to age-related cataract through the p62/Keap1/Nrf2 signaling pathway-mediated ferroptosis. This research is relevant as it explores a potential mechanism underlying a specific age-related disease, which could inform strategies for addressing the biological processes of aging.

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