ReviewBiomolecules2022
Mitochondrial Dysfunction in Rheumatoid Arthritis.
Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
What it found
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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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Mitochondria: a breakthrough in combating rheumatoid arthritis.Frontiers in medicine · 2024Pooled it
- Mitochondrial Communication Networks in the Bone Microenvironment: From the Maintenance of Homeostasis to Translational Interventions for Bone Diseases.Stem cell reviews and reports · 2026Review
- Antiglycation approach in selected autoimmune diseases: Where do we stand?Redox biology · 2026Review
- Patient-Derived Transcriptomics Reveals Distinct IFNγ-Associated Myeloid States and Mitochondrial Complex I Programs in Rheumatoid Arthritis and Osteoarthritis.Biomedicines · 2026Article
- Metabolic exhaustion and immune ageing in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Immune responses in aging adults.The Journal of clinical investigation · 2026Review
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Article
- Mitochondria as an Integrative Hub of Cellular Homeostasis and Stress Response.International journal of molecular sciences · 2026Review
- ANGPTL2 inhibits macrophage pyroptosis and alleviates rheumatoid arthritis progression by regulating mitophagy via IGFBP5.Cell death & disease · 2026Article
- GFER Represents a Target for Dual Disruption of Redox Homeostasis and Reactivation of the Immune Response in Pancreatic Adenocarcinoma.Cancer research · 2026Article
- Exploring the Shared Diagnostic Biomarkers and Molecular Mechanisms Related to Mitochondrial Dysfunction in Inflammatory Bowel Disease and Rheumatoid Arthritis.Current issues in molecular biology · 2026Article
- Mitochondrial Hub Genes in Rheumatoid Arthritis Identified by Machine Learning and Mendelian Randomization with Experimental Validation.Journal of inflammation research · 2026Article
- Exosomal non-coding RNAs in autoimmune diseases: molecular mechanisms and potential applications.Frontiers in immunology · 2026Review
- Therapeutic Nanozymes in Rheumatoid Arthritis Treatment Through Disease Stage-Oriented Strategies.International journal of nanomedicine · 2026Review
- Connection Between Mitochondria and Rheumatoid Arthritis and Osteoarthritis: Personalized Treatment Strategies.Current pharmaceutical design · 2026Review
- Bone marrow mesenchymal stem cell-derived exosomes improve pyroptosis and mitochondrial integrity through miR-515-5p-mediated TLR4/NLRP3/GSDMD axis in rheumatoid arthritis.Arthritis research & therapy · 2025Article
- Review
- Functionalized hydrocaffeic acid-chitosan/EGTA hydrogel rescues mitochondrial dysfunction for immunomodulation and joint repair in rheumatoid arthritis.Materials today. Bio · 2025Article
- Salidroside: A Potential Drug Candidate to Treat Rheumatoid Arthritis.Molecules (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis, a chronic autoimmune disease with complex etiology, is characterized by excessive proliferation of synovial cells, massive production of inflammatory cells and cartilage destruction. Studies have shown that mitochondrial dysfunction plays an important role in promoting the occurrence of RA. Mitochondria with normal structure and function are essential for the normal survival of chondrocytes and synovial cells. Once mitochondrial function is destroyed, it will affect the survival, activation and differentiation of immune cells and non-immune cells involved in the pathogenesis of RA, thus leading to the occurrence of RA. However, the mechanism of mitochondrial dysfunction in RA remains unclear. This article reviews the method of mitochondrial dysfunction leading to RA, the effects of mitochondrial dysfunction on immune cells, the etiology of mitochondrial dysfunction in RA, and the pathology of mitochondrial dysfunction in RA. We also outline some drugs that can exert therapeutic effects on RA which are associated with modulating mitochondrial activity. The understanding and summary of mitochondrial dysfunction in RA may provide new research directions for pathological intervention and prevention of RA.
Indexed as
Identifiers
What 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.