Published online Mar 15, 2024. doi: 10.4239/wjd.v15.i3.519
Peer-review started: October 12, 2023
First decision: December 6, 2023
Revised: December 8, 2023
Accepted: January 18, 2024
Article in press: January 18, 2024
Published online: March 15, 2024
Processing time: 154 Days and 21.8 Hours
Diabetic retinopathy (DR) is a major ocular complication of diabetes mellitus, leading to visual impairment. Retinal pigment epithelium (RPE) injury is a key component of the outer blood retinal barrier, and its damage is an important indicator of DR.
Therefore, inhibiting receptor for activated C kinase 1 (RACK1) may be a potential therapeutic strategy to slow down the progression of early DR by regulating protein kinase C-ε/ reactive oxygen species (PKC-ε/ROS).
Knockdown of RACK1 can reduce the activity of PKC-ε and the production of ROS, thereby alleviating cellular oxidative stress and inflammatory responses. By reducing the excessive activation of PKC-ε/ROS, the occurrence and progression of early DR can be reduced.
In this study, Sprague-Dawley rats and adult RPE cell line-19 (ARPE-19) cells were used as in vivo and in vitro models, respectively, to explore the role of RACK1 in mediating PKC-ε in early DR. Furthermore, the effect on the apoptosis and barrier function of RPE cells was also investigated in the former model.
Knockdown of RACK1 can reduce the activity of PKC-ε and the production of ROS, thereby alleviating cellular oxidative stress and inflammatory responses. By reducing the excessive activation of PKC-ε/ROS, the occurrence and progression of early DR can be reduced.
this study proposes that by reducing the excessive activation of PKC-ε/ROS, the occurrence and progression of early DR can be reduced. This may be achieved through the reduction of cellular oxidative stress and inflammatory response, improvement of retinal cell survival and function, and the reduction of vascular lesions and inflammatory infiltration.
One of the main limitations of this study is that all the mechanistic experiments were conducted in ARPE-19 cells. Future studies need to confirm the effect of RACK1 on the oBRB in diabetic rats.