Purchase this article with an account.
Xueting Luo, Xiangjun She, Xinmin Lu, Xiaodong Sun; Mitochondrial Dysfunction in Photoreceptors after Retinal Detachment. Invest. Ophthalmol. Vis. Sci. 2018;59(9):967.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To dissect the mechanism underlying photoreceptor degeneration after retinal detachment.
The vitreous from patients with retinal detachment was analyzed by quantitative metabolics. A rat model of retinal detachment and cultured photoreceptors subjected to oxidative stress were also employed to interrogate underlying molecular mechanisms.
Key metabolites in the glycolytic pathway were dysregulated in the vitreous of patients with retinal detachment. In the animal models, We showed that retinal detachment activated dynamin-related protein 1 dependent mitochondrial fission, ROS release and apoptotic cascades. Pharmacological blockade or RNA interference of dynamin-related protein 1 activity preserved mitochondrial integrity, attenuated ROS production and rescued photoreceptors both in vivo and in vitro.
Our findings have identified mitochondrial fission as a critical ‘danger signal’ to photoreceptor degeneration and dynamin-related protein 1 as a promising therapeutic target for photoreceptor protection after retinal detachment.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
This PDF is available to Subscribers Only