DCLRE1 downregulated by SYVN1-mediated ubiquitination and degradation, weakening mitochondrial homeostasis protection in ARC formation.

Tianyu Cheng, Pengfei Li, Jiancen Tang, Hongping Cui, Jierui Jia, Lu Wang, Qian Li

Department of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.Department of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China. · pubmed

Paper

Abstract

DNA oxidative damage of lens epithelium cells (LECs) has been proved to be significantly related to age-related cataract (ARC). DCLRE1A, as a member of the DNA interstrand cross-links pathway, can repair damaged DNA. However, DCLRE1A has not been addressed in maintaining mitochondrial healthy. Our findings demonstrated that DCLRE1A alleviated mtDNA oxidative damage and mitochondrial dysfunction. Besides, the E3 ubiquitin ligase SYVN1 interacts with DCLRE1A and promotes its ubiquitination and degradation. Furthermore, SYVN1 knockdown exacerbated H

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Research summary

DCLRE1A plays a protective role against mitochondrial dysfunction and oxidative damage in lens epithelium cells. The study addresses a mechanism related to mitochondrial health, which is crucial for understanding age-related diseases like cataracts, thus contributing to the broader field of longevity research.

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