ArticleCell death & disease2019
Mitochondrial 3243A > G mutation confers pro-atherogenic and pro-inflammatory properties in MELAS iPS derived endothelial cells.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- The Role of Estrogen in Mitochondrial Disease.Cellular and molecular neurobiology · 2025Pooled it
- Metabolomic signature reveals dysregulated lipoprotein profile in m.3243A>G carriers: a case-control study.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Review
- Cholesterol in Mitochondrial Diseases-Friend or Foe?International journal of molecular sciences · 2026Review
- The Emerging Role of N-Lactoyl-Phenylalanine (Lac-Phe) in Metabolic Regulation and Disease: From Exercise-Induced Metabolite to Therapeutic Candidate.Antioxidants (Basel, Switzerland) · 2026Article
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- Pathogenic role of mitochondrial DNA mutations in heart failure: clinical features, mechanisms, and therapeutic prospects.Frontiers in cardiovascular medicine · 2026Review
- Mitochondrial Mutation Leads to Cardiomyocyte Hypertrophy by Disruption of Mitochondria-Associated ER Membrane.Cell proliferation · 2025Article
- Metabolic remodeling in hiPSC-derived myofibers carrying the m.3243A>G mutation.Stem cell reports · 2025Article
- Efficacy and Safety of Photobiomodulation in MELAS: Protocol for a Series of N-of-1 Trials.Journal of clinical medicine · 2025Article
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Mitochondrial Chronic Progressive External Ophthalmoplegia.Brain sciences · 2024Review
- Induced pluripotent stem cells: ex vivo models for human diseases due to mitochondrial DNA mutations.Journal of biomedical science · 2023Review
- The Mitochondrial m.3243A>G Mutation on the Dish, Lessons from In Vitro Models.International journal of molecular sciences · 2023Review
- Multimodal single-cell analysis of nonrandom heteroplasmy distribution in human retinal mitochondrial disease.JCI insight · 2023Article
- Identification of peripheral vascular function measures and circulating biomarkers of mitochondrial function in patients with mitochondrial disease.Clinical and translational science · 2023Article
- Modeling mitochondrial DNA diseases: from base editing to pluripotent stem-cell-derived organoids.EMBO reports · 2023Review
- Role of the mtDNA Mutations and Mitophagy in Inflammaging.International journal of molecular sciences · 2022Review
- Mitochondrial Dysfunction in Cardiovascular Diseases: Potential Targets for Treatment.Frontiers in cell and developmental biology · 2022Review
- Clinical features, pathogenesis, and management of stroke-like episodes due to MELAS.Metabolic brain disease · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a mitochondrial disorder that is commonly caused by the m.3243A > G mutation in the MT-TL1 gene encoding for mitochondrial tRNA(Leu(UUR)). While clinical studies reported cerebral infarcts, atherosclerotic lesions, and altered vasculature and stroke-like episodes (SLE) in MELAS patients, it remains unclear how this mutation causes the onset and subsequent progression of the disease. Here, we report that in addition to endothelial dysfunction, diseased endothelial cells (ECs) were found to be pro-atherogenic and pro-inflammation due to high levels of ROS and Ox-LDLs, and high basal expressions of VCAM-1, in particular isoform b, respectively. Consistently, more monocytes were found to adhere to MELAS ECs as compared to the isogenic control, suggesting the presence of an atherosclerosis-like pathology in MELAS. Notably, these disease phenotypes in endothelial cells can be effectively reversed by anti-oxidant treatment suggesting that the lowering of ROS is critical for treating patients with MELAS syndrome.
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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.