ArticleMiddle East African journal of ophthalmology2011
Leber's Hereditary Optic Neuropathy: The Mitochondrial Connection Revisited.
Article in Middle East African journal of ophthalmology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- The pathological mechanisms and novel therapeutics for Leber's hereditary optic neuropathy.Journal of the Chinese Medical Association : JCMA · 2023Article
- The epidemiology and mutation types of Leber's hereditary optic neuropathy in Thailand.Annals of medicine · 2022Article
- Retinal Circular RNA hsa_circ_0087207 Expression Promotes Apoptotic Cell Death in Induced Pluripotent Stem Cell-Derived Leber's Hereditary Optic Neuropathy-like Models.Biomedicines · 2022Article
- Frequency of primary mutations of Leber's hereditary optic neuropathy patients in North Indian population.Indian journal of ophthalmology · 2017Observational
- Profound vision loss impairs psychological well-being in young and middle-aged individuals.Clinical ophthalmology (Auckland, N.Z.) · 2017Article
- Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids.PloS one · 2016Article
- Analyses of the mitochondrial mutations in the Chinese patients with sporadic Creutzfeldt-Jakob disease.European journal of human genetics : EJHG · 2015Article
- Clinical and electrophysiological recovery in Leber hereditary optic neuropathy with G3460A mutation.Documenta ophthalmologica. Advances in ophthalmology · 2012Article
- Ophthalmic genetics: moving forward.Middle East African journal of ophthalmology · 2011Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our current understanding of Leber's hereditary optic neuropathy (LHON)-mitochondrial connection falls short of comprehensive. Twenty years of intensive investigation have yielded a wealth of information about mitochondria, the mitochondrial genome, the metabolism of the optic nerve and other structures, and the phenotypic variability of classic LHON. However, we still cannot completely explain how primary LHON mutations injure the optic nerve or why the optic nerve is particularly at risk. We cannot explain the incomplete penetrance or the male predominance of LHON, the typical onset in young adult life without warning, or the synchronicity of visual loss. Moreover, primary LHON mutations clearly are not present in every family with the LHON phenotype (including multigenerational maternal inheritance), and they are present in only a minority of individuals who have the LHON optic neuropathy phenotype without a family history. All lines of evidence point to abnormalities of the mitochondria as the direct or indirect cause of LHON. Therefore, the mitochondria-LHON connection needs to be revisited and examined closely. This review will attempt to do that and provide an update on various aspects of LHON.
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Registered trials
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