Neuroprotective Strategy in Retinal Degeneration: Suppressing ER Stress-Induced Cell Death via Inhibition of the mTOR Signal

被引:14
作者
Fan, Bin [1 ]
Sun, Ying-Jian [1 ]
Liu, Shu-Yan [1 ]
Che, Lin [1 ]
Li, Guang-Yu [1 ]
机构
[1] Jilin Univ, Dept Ophthalmol, Hosp 2, Changchun 130041, Peoples R China
基金
中国国家自然科学基金;
关键词
mTOR; ER stress; retinal degeneration; unfolded protein response; retinal neuroprotection; apoptosis; ENDOPLASMIC-RETICULUM STRESS; MESSENGER-RNA TRANSLATION; MUTANT ELOVL4; BETA-SUBUNIT; PROTEIN; GENE; MODEL; RAPAMYCIN; PATHWAYS; MUTATION;
D O I
10.3390/ijms18010201
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The retina is a specialized sensory organ, which is essential for light detection and visual formation in the human eye. Inherited retinal degenerations are a heterogeneous group of eye diseases that can eventually cause permanent vision loss. UPR (unfolded protein response) and ER (endoplasmic reticulum) stress plays an important role in the pathological mechanism of retinal degenerative diseases. mTOR (the mammalian target of rapamycin) kinase, as a signaling hub, controls many cellular processes, covering protein synthesis, RNA translation, ER stress, and apoptosis. Here, the hypothesis that inhibition of mTOR signaling suppresses ER stress-induced cell death in retinal degenerative disorders is discussed. This review surveys knowledge of the influence of mTOR signaling on ER stress arising from misfolded proteins and genetic mutations in retinal degenerative diseases and highlights potential neuroprotective strategies for treatment and therapeutic implications.
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页数:14
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