4-Acetoxyphenol Prevents RPE Oxidative Stress–Induced Necrosis by Functioning as an NRF2 Stabilizer | Zendy

Jakub Hanus | Zendy; Alexander Kolkin | Zendy; Julia Chimienti | Zendy; Sara Botsay | Zendy; Shusheng Wang | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

4-Acetoxyphenol Prevents RPE Oxidative Stress–Induced Necrosis by Functioning as an NRF2 Stabilizer

Author(s) -

Jakub Hanus,

Alexander Kolkin,

Julia Chimienti,

Sara Botsay,

Shusheng Wang

Publication year - 2015

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.15-16401

Subject(s) - oxidative stress , reactive oxygen species , viability assay , microbiology and biotechnology , chemistry , apoptosis , programmed cell death , transfection , necrosis , antioxidant , downregulation and upregulation , keap1 , pharmacology , biochemistry , biology , transcription factor , gene , genetics

Oxidative stress has been suggested to be a major risk factor for the pathogenesis of AMD. Retinal pigment epithelial (RPE) cells are essential for maintaining the homeostasis of the retina, and RPE cell death and the resultant photoreceptor apoptosis have been observed in dry AMD, especially in geographic atrophy. The purpose of this article was to identify and repurpose the Food and Drug Administration-approved natural compound 4-Acetoxyphenol (4-AC), and to evaluate its effect and mechanism in protecting against oxidative stress-induced RPE necrosis.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research