ArticleClinical immunology (Orlando, Fla.)2008
Association of common mitochondrial DNA variants with multiple sclerosis and systemic lupus erythematosus.
Article in Clinical immunology (Orlando, Fla.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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.
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.
Who cites it
45 citing papers in PubMed, 88 citations in OpenAlex.
- Leukocyte mitochondrial DNA alteration in systemic lupus erythematosus and its relevance to the susceptibility to lupus nephritis.International journal of molecular sciences · 2012Trial
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- Mitochondrial tRNA-Derived Diseases.International journal of molecular sciences · 2025Review
- Genomic ncRNAs regulating mitochondrial function in neurodegeneration: a neglected clue in the complex etiopathogenesis of multiple sclerosis.Cell & bioscience · 2025Article
- The PP2A regulatory subunit PPP2R2A controls NADCell reports · 2024Article
- CD4Scientific reports · 2024Article
- Screening for Mitochondrial tRNA Variants in 200 Patients with Systemic Lupus Erythematosus.Human heredity · 2024Article
- Advances in the Pathogenesis and Treatment of Systemic Lupus Erythematosus.International journal of molecular sciences · 2023Review
- The complexities of investigating mitochondria dynamics in multiple sclerosis and mouse models of MS.Frontiers in neuroscience · 2023Review
- The role of mitochondria in rheumatic diseases.Nature reviews. Rheumatology · 2022Review
- CD4Precision clinical medicine · 2022Review
- Performance of a Standardized Clinical Assay for Urinary C-C Motif Chemokine Ligand 14 (CCL14) for Persistent Severe Acute Kidney Injury.Kidney360 · 2022Article
- Isolevuglandins disrupt PU.1-mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus.JCI insight · 2022Article
- Analysis of the entire mitochondrial genome reveals Leber's hereditary optic neuropathy mitochondrial DNA mutations in an Arab cohort with multiple sclerosis.Scientific reports · 2022Article
- Mitochondria in the Pathogenesis of Systemic Lupus Erythematosus.Current rheumatology reports · 2022Review
- Article
- Mitochondrial DNA haplogroup analysis in Saudi Arab patients with multiple sclerosis.PloS one · 2022Article
- Type I interferons affect the metabolic fitness of CD8Nature communications · 2021Article
- Oxidative/Nitroxidative Stress and Multiple Sclerosis.Journal of molecular neuroscience : MN · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction has been implicated in the pathogenesis of multiple sclerosis (MS) and systemic lupus erythematosus (SLE). This study re-investigates the roles of previously suggested candidate genes of energy metabolism (Complex I genes located in the nucleus and in the mitochondria) in patients with MS relative to ethnically matched SLE patients and healthy controls. After stringent correction for multiple testing, we reproduce the association of the mitochondrial (mt)DNA haplotype K* with MS, but reject the importance of previously suggested borderline associations with nuclear genes of Complex I. In addition, we detect the association of common variants of the mitochondrial ND2 and ATP6 genes with both MS and SLE, which raises the possibility of a shared mitochondrial genetic background of these two autoimmune diseases.
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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.