mTORC2 activation protects retinal ganglion cells via Akt signaling after autophagy induction in traumatic optic nerve injury

Abstract

Eye disease: switching signals for repairing injured optic nerves Regulating molecular signaling pathways that control the degradation of cellular components—a process known as autophagy—could offer a new approach to treating optic nerve damage after traumatic injuries. There is currently no established treatment option for traumatic optic nerve injury. Rong-Kung Tsai and colleagues at Tzu Chi University in Hualien, Taiwan, explored the role of a protein complex called mTORC2 in autophagy during the repair of optic nerves in rats. They investigated mTORC2 activation by small RNA molecules that also activate autophagy, and by drugs that activate autophagy but inhibit mTORC2. The results indicate that autophagy associated with activation of mTORC2 protects damaged retinal neurons and promotes visual recovery. In addition to treating optic nerve injuries, drugs activating mTORC2 and autophagy might help treat nerve-related diseases of the eye, including glaucoma.