ReviewJournal of molecular medicine (Berlin, Germany)2024
Progress in diagnosis and treatment of Leber's hereditary optic neuropathy.
Review in Journal of molecular medicine (Berlin, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Elevated iron levels in tears of patients diagnosed with WDR45 X-linked optic atrophy.Orphanet journal of rare diseases · 2026Article
- A multistage cost-effective strategy for the molecular diagnosis of unexplained vision loss patients: practice in inherited ocular fundus disease.Molecular genetics and genomics : MGG · 2026Article
- Genetic Features and Clinical Heterogeneity of Leber Hereditary Optic Neuropathy in Adolescent and Adult Patients: A Case Series on Arab Patients.International medical case reports journal · 2026Article
- Biological and translational attributes of mitochondrial DNA copy number: Laboratory perspective to clinical relevance.World journal of methodology · 2025Review
- Early Macular Ganglion Cell Loss in Leber Hereditary Optic Neuropathy, an Optical Coherence Tomography Biomarker to Differentiate Optic Neuritis.Journal of clinical medicine · 2025Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Leber's hereditary optic neuropathy (LHON) is a mitochondrial genetic disease with central vision loss as the main symptom. It is one of the diseases that cause vision loss and optic atrophy in young and middle-aged people. The mutations of these three primary mitochondrial mutations, m.11778G>A, m.14484T>C, and m.3460G>A, are the main molecular basis, but their pathogenesis is also affected by nuclear genes, mitochondrial genetic background, and environmental factors. This article summarizes the research progress on molecular pathogenesis, clinical symptoms, and treatment of LHON in recent years, aiming to summarize the genetic pathogenesis and clinical treatment points of LHON.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.