Increasing mtDNA levels as therapy for mitochondrial optic neuropathies.

Increasing mtDNA levels as therapy for mitochondrial optic neuropathies. Drug Discov Today. 2018 Jan 11;: Authors: Ruiz-Pesini E, Emperador S, López-Gallardo E, Hernandez-Ainsa C, Montoya J Abstract Leber hereditary optic neuropathy (LHON) is a rare, inherited mitochondrial disease. No treatment has shown a clear-cut benefit on a clinically meaningful end-point. Primary open-angle glaucoma is a frequent, acquired optic neuropathy. Lowering intraocular pressure reduces disease progression. However, current methods to decelerate this progression are recognized as being inadequate. Therefore, there is a clear need to look for new therapeutic approaches. The growing evidence indicates that primary open-angle glaucoma can also be a mitochondrial optic neuropathy (MON). Several risk elements are common for both diseases and all of them decrease mitochondrial (mt)DNA content. Based on these susceptibility factors and their molecular mechanism, we suggest herein pharmacological therapies targeted to increase mtDNA levels, oxidative phosphorylation capability, and mitochondrial energy production as treatments for MONs. PMID: 29337205 [PubMed - as supplied by publisher]
Source: Drug Discovery Today - Category: Drugs & Pharmacology Authors: Tags: Drug Discov Today Source Type: research