ArticleJournal of lipid and atherosclerosis2024
Mitochondrial Genome Editing: Exploring the Possible Relationship of the Atherosclerosis-Associated Mutation m.15059G>A With Defective Mitophagy.
Article in Journal of lipid and atherosclerosis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed.
- Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026Review
- Mitochondrial Dysfunction Associated with mtDNA Mutation: Mitochondrial Genome Editing in Atherosclerosis Research.Current medicinal chemistry · 2026Article
- Reprogramming the Mitochondrion in Atherosclerosis: Targets for Vascular Protection.Antioxidants (Basel, Switzerland) · 2025Review
- Carrier-free self-assembled nanomedicines of active ingredients from pomegranate peel: an overview.Discover nano · 2025Review
- The Role of mtDNA Mutations in Atherosclerosis: The Influence of Mitochondrial Dysfunction on Macrophage Polarization.International journal of molecular sciences · 2025Review
- Review
- Mitochondrial DNA Mutations as a Factor in the Heritability of Atherosclerosis and Other Diseases.Current medicinal chemistry · 2025Review
- Defective Mitophagy Impairs Response to Inflammatory Activation of Macrophage-Like Cells.Current medicinal chemistry · 2025Article
- Evidence for the Involvement of Gene Regulation of Inflammatory Molecules in the Accumulation of Intracellular Cholesterol: The Mechanism of Foam Cell Formation in Atherosclerosis.Current medicinal chemistry · 2025Article
- Molecular Aspects of Inflammation and Lipid Metabolism in Health and Disease: The Role of the Mitochondria.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: The aim of this study was to evaluate the effect of the m.15059G>A mitochondrial nonsense mutation on cellular functions related to atherosclerosis, such as lipidosis, pro-inflammatory response, and mitophagy. Heteroplasmic mutations have been proposed as a potential cause of mitochondrial dysfunction, potentially disrupting the innate immune response and contributing to the chronic inflammation associated with atherosclerosis. Methods: The human monocytic cell line THP-1 and cytoplasmic hybrid cell line TC-HSMAM1 were used. An original approach based on the CRISPR/Cas9 system was developed and used to eliminate mitochondrial DNA (mtDNA) copies carrying the m.15059G>A mutation in the Results: In contrast to intact TC-HSMAM1 cybrids, Cas9-TC-HSMAM1 cells exhibited a decrease in fatty acid synthase ( Conclusion: The m.15059G>A mutation was found to be associated with defective mitophagy, immune tolerance, and impaired metabolism of intracellular lipids due to upregulation of
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