KLF10-IN-1 Attenuates RPE Cell Apoptosis and Experimental Diabetic Retinopathy Via the KLF10/PERK/eIF2α/ATF4/CHOP Pathway.

ABSTRACT:

Purpose

To investigate the roles of Krüppel-like factor 10 (KLF10) and its inhibitor KLF10-IN-1 in regulating high-glucose/hypoxia-induced RPE cell apoptosis and their involvement in diabetic retinopathy (DR).

Methods

A DR mouse model was established using a high-fat, high-glucose diet and streptozotocin. An RPE cell model of high-glucose/hypoxia injury was constructed by culturing cells under high-glucose (30 mM) conditions in the presence of cobalt chloride (200 µM). KLF10 expression, apoptosis, and endoplasmic reticulum (ER) stress levels were assessed. KLF10 expression was modulated with small interfering RNA and overexpression plasmids. Dual luciferase reporter assays were used to evaluated the regulatory effect of KLF10 on PERK. The PERK pathway was activated by CCT020

SUBMITTER: Hu W 

PROVIDER: S-EPMC12700178 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature