Evidence map›Paper›PMID 40332750›Full record

ReviewInternational journal of molecular sciences2025

Isolated and Syndromic Genetic Optic Neuropathies: A Review of Genetic and Phenotypic Heterogeneity.

Marco Zeppieri, Caterina Gagliano, Marco Di Maita, Alessandro Avitabile, Giuseppe Gagliano, Edoardo Dammino, Daniele Tognetto, Maria Francesca Cordeiro, Fabiana D'Esposito

Erratum issuedAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Marco ZeppieriDepartment of Ophthalmology, University Hospital of Udine, 33100 Udine, Italy.ORCID 0000-0003-0999-5545
Caterina GaglianoDepartment of Medicine and Surgery, "Kore" University of Enna, Piazza dell'Università, 94100 Enna, Italy.ORCID 0000-0001-8424-0068
Marco Di MaitaMediterranean Foundation "G.B. Morgagni", Via Sant'Euplio, 95100 Catania, Italy.ORCID 0000-0001-9868-6570
Alessandro AvitabileEye Clinic Catania University San Marco Hospital, Viale Carlo Azeglio Ciampi, 95121 Catania, Italy.ORCID 0009-0003-1051-876X
Giuseppe GaglianoEye Clinic Catania University San Marco Hospital, Viale Carlo Azeglio Ciampi, 95121 Catania, Italy.ORCID 0009-0006-0059-5253
Edoardo DamminoEye Clinic Catania University San Marco Hospital, Viale Carlo Azeglio Ciampi, 95121 Catania, Italy.
Daniele TognettoDepartment of Medicine, Surgery and Health Sciences, University of Trieste, 34127 Trieste, Italy.
Maria Francesca CordeiroImperial College Ophthalmic Research Group (ICORG) Unit, Imperial College, 153-173 Marylebone Rd, London NW1 5QH, UK.
Fabiana D'EspositoImperial College Ophthalmic Research Group (ICORG) Unit, Imperial College, 153-173 Marylebone Rd, London NW1 5QH, UK.ORCID 0000-0002-7938-876X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonsyndromic and syndromic hereditary optic neuropathies (HONs) encompass a variety of genetic illnesses that cause progressive optic nerve damage, resulting in considerable vision impairment. These disorders result from pathogenic variants in mitochondrial or nuclear DNA, impacting essential cellular processes like oxidative phosphorylation, mitochondrial dynamics, and neuroprotection. Advances in next-generation sequencing (NGS) have significantly improved the identification of genetic variations, enabling precise diagnoses and genotype-phenotype correlations. This review consolidates current knowledge regarding the classification, molecular pathogenesis, clinical manifestations, diagnostic methodologies, and emerging therapeutic strategies for HONs. The critical role of mitochondrial dysfunction in optic nerve degeneration highlights the necessity for multimodal therapeutic approaches. Recent clinical trials evaluating gene therapy for Leber hereditary optic neuropathy (LHON) and neuroprotective strategies in dominant optic atrophy (DOA) are discussed. Additionally, individualized therapeutic interventions, as demonstrated by recent case studies involving tailored gene therapies, are evaluated. The integration of molecular and imaging biomarkers in future personalized treatment strategies aims to enhance prognosis and therapeutic outcomes.

Indexed as

Genetic HeterogeneityOptic Nerve DiseasesDNA, MitochondrialGenetic Association StudiesGenetic TherapyHumansMutationOptic Atrophy, Hereditary, LeberPhenotypeDNA, Mitochondrialdominant optic atrophy (DOA)gene therapyhereditary optic neuropathyLeber hereditary optic neuropathy (LHON)mitochondrial DNAoptic atrophywolfram syndrome

Identifiers

PMID40332750
PMCPMC12027957

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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.