Open AccessNrf2 as a target for prevention of age‐related and diabetic cataracts by against oxidative stress
Author(s) -
Liu XiuFen,
Hao JiLong,
Xie Tian,
Malik Tayyab Hamid,
Lu ChengBo,
Liu Cong,
Shu Chang,
Lu ChengWei,
Zhou DanDan
Publication year - 2017
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.12645
Subject(s) - oxidative stress , cataracts , blindness , biology , keap1 , oxidative phosphorylation , microbiology and biotechnology , bioinformatics , medicine , biochemistry , genetics , optometry , transcription factor , gene
Summary Cataract is one of the most important causes of blindness worldwide, with age‐related cataract being the most common one. Agents preventing cataract formation are urgently required. Substantial evidences point out aggravated oxidative stress as a vital factor for cataract formation. Nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2)/Kelch‐like erythroid‐cell‐derived protein with CNC homology ( ECH )‐associated protein 1 (Keap1) system is considered as one of the main cellular defense mechanisms against oxidative stresses. This review discusses the role of Nrf2 pathway in the prevention of cataracts and highlights that Nrf2 suppressors may augment oxidative stress of the lens, and Nrf2 inducers may decrease the oxidative stress and prevent the cataract formation. Thus, Nrf2 may serve as a promising therapeutic target for cataract treatment.