Abstract
Leber hereditary optic neuropathy (LHON) is a maternally transmitted hereditary disease. Mitochondrial dysfunction and stress are involved in the degeneration and apoptosis of retinal ganglion cells (RGCs). The continuous innovation and improvement of the LHON models provide a good experimental basis for the study of the molecular mechanism of LHON. Among them, the ectopically expressed LHON mutant cells are the main research tools at this stage. Gene therapy is a breakthrough point in the treatment of LHON which has been tested in the clinic. (Int Rev Ophthalmol, 2018, 42: 302-306) Key words: Leber hereditary optic neuropathy; mitochondrion; models; therapy
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
