ReviewMolecular neurobiology2024
Cellular and Molecular Responses to Mitochondrial DNA Deletions in Kearns-Sayre Syndrome: Some Underlying Mechanisms.
Review in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Review
- UVA Irradiation Promotes ROS-Mediated Formation of the Common Deletion in Mitochondrial DNA.Life (Basel, Switzerland) · 2026Article
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Mapping Disorders with Neurological Features Through Mitochondrial Impairment Pathways: Insights from Genetic Evidence.Current issues in molecular biology · 2025Review
- Syndromic Retinitis Pigmentosa: A Narrative Review.Vision (Basel, Switzerland) · 2025Review
- Molecular Aspects of Mitochondrial Dysfunction in Diabetes, Pearson and Kearns-Sayre Syndromes, and Neurodegenerative Disorders.International journal of general medicine · 2025Review
- Aberrant ER-mitochondria communication is a common pathomechanism in mitochondrial disease.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
Kearns-Sayre syndrome (KSS) is a rare multisystem mitochondrial disorder. It is caused by mitochondrial DNA (mtDNA) rearrangements, mostly large-scale deletions of 1.1-10 kb. These deletions primarily affect energy supply through impaired oxidative phosphorylation and reduced ATP production. This impairment gives rise to dysfunction of several tissues, in particular those with high energy demand like brain and muscles. Over the past decades, changes in respiratory chain complexes and energy metabolism have been emphasized, whereas little attention has been paid to other reports on ROS overproduction, protein synthesis inhibition, myelin vacuolation, demyelination, autophagy, apoptosis, and involvement of lipid raft and oligodendrocytes in KSS. Therefore, this paper draws attention towards these relatively underemphasized findings that might further clarify the pathologic cascades following deletions in the mtDNA.
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Registered trials
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