ReviewCurrent rheumatology reports2022
Mitochondria in the Pathogenesis of Systemic Lupus Erythematosus.
Review in Current rheumatology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled 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.
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Metabolic determinants of autoimmune kidney diseases.Nature reviews. Nephrology · 2026Review
- Persistent symptom burden in long-standing systemic lupus erythematosus: a subgroup-focused hypothesis for an SLE-ME/CFS research phenotype.Journal of translational medicine · 2026Article
- Fatigue beyond inflammation in inflammatory rheumatic diseases: a narrative review and treatable-traits framework.Rheumatology international · 2026Review
- Interferon-alpha selectively signals mitochondrial pore opening to allow mitochondrial RNA release in systemic lupus erythematosus: pathophysiological implications.Cell communication and signaling : CCS · 2026Article
- Integrated bioinformatics and clinical validation reveals PRDX6 as a mitochondrial hub gene in systemic lupus erythematosus.Clinical rheumatology · 2026Article
- Identification of key oxidative phosphorylation-related genes in systemic lupus erythematosus based on transcriptomics and bioinformatics analysis.Journal of translational autoimmunity · 2025Article
- Distinction Between Proliferative Lupus Nephritis and Membranous Lupus Nephritis Based on Inflammation, NETosis, and Glomerular Exostosin.International journal of molecular sciences · 2025Review
- Platelets and diseases: signal transduction and advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Induction of LY6E regulates interleukin-1β production, potentially contributing to the immunopathogenesis of systemic lupus erythematosus.Cell communication and signaling : CCS · 2025Article
- Cell-free DNA: a metabolic byproduct with diagnostic and prognostic potential in rheumatic disorders.Frontiers in pharmacology · 2025Review
- Identification of mitochondrial function and programmed cell death associated key biomarkers and the circRNA-miRNA-mRNA regulatory network in systemic lupus erythematosus.Frontiers in molecular biosciences · 2025Article
- Mitochondrial mass and mitochondrial membrane potential of peripheral lymphocytes: promising biomarkers of systemic lupus erythematosus.Frontiers in molecular biosciences · 2025Article
- Plasma cell-free DNA genome-wide methylation profiling enables detection and activity assessment in systemic lupus erythematosus.Frontiers in immunology · 2025Article
- CMPK2 Promotes CD4Cell biochemistry and biophysics · 2024Article
- Mechanisms underlying sex differences in autoimmunity.The Journal of clinical investigation · 2024Review
- Multiple polygenic risk scores can improve the prediction of systemic lupus erythematosus in Taiwan.Lupus science & medicine · 2024Article
- Review
- Therapeutically targeting proinflammatory type I interferons in systemic lupus erythematosus: efficacy and insufficiency with a specific focus on lupus nephritis.Frontiers in immunology · 2024Review
- Mitochondrial extracellular vesicles, autoimmunity and myocarditis.Frontiers in immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewSystemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production and inflammation in multiple organs. In this article, we present data on how various mitochondria pathologies are involved in the pathogenesis of the disease including the fact that they serve as a reservoir of autoantigens which contribute to the upending of lymphocyte tolerance. RECENT
findingsMitochondrial DNA from various cell sources, including neutrophil extracellular traps, platelets, and red blood cells, elicits the production of type I interferon which contributes to breaking of peripheral tolerance. Mitochondrial DNA also serves as autoantigen targeted by autoantibodies. Mutations of mitochondrial DNA triggered by reactive oxygen species induce T cell cross-reactivity against self-antigens. Selective gene polymorphisms that regulate mitochondrial apoptosis in autoreactive B and T cells represent another key aspect in the induction of autoimmunity. Various mitochondrial abnormalities, including changes in mitochondrial function, oxidative stress, genetic polymorphism, mitochondrial DNA mutations, and apoptosis pathways, are each linked to different aspects of lupus pathogenesis. However, whether targeting these mitochondrial pathologies can be used to harness autoimmunity remains to be explored.
Indexed as
Identifiers
35290598What OpenQuestion holds
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.