ReviewJournal of inflammation research2024
Important Role of Mitochondrial Dysfunction in Immune Triggering and Inflammatory Response in Rheumatoid Arthritis.
Review in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- Reprogramming Neuroinflammation: Mitochondrial Targets and Immune Checkpoint Inhibitors in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Metformin as a Metabolic Reprogramming Interface in Host-Pathogen and Bone Microenvironment Crosstalk: A Dual-Target Strategy Against Antimicrobial Resistance and Osteoporotic Bone Loss.Antibiotics (Basel, Switzerland) · 2026Review
- Geroscience insights into difficult-to-treat rheumatoid arthritis: the role of unhealthy aging, comorbidity, and therapeutic complexity.GeroScience · 2026Review
- Targeting mitochondrial oxidative stress: A novel therapeutic strategy for degenerative joint diseases (Review).Biomedical reports · 2026Review
- Gut Microbial Composition, Oxidative Stress, and Immunity in Metabolic Disease: Toward Personalized Interventions.Antioxidants (Basel, Switzerland) · 2026Review
- Intercellular mitochondrial transfer in melanoma progression and therapeutic resistance: mechanisms and targeting potential.Frontiers in oncology · 2026Review
- Mitochondrial Dysfunction and Metabolic Reprogramming in Chronic Inflammatory Diseases: Molecular Insights and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
- Integration of mitochondrial gene expression and immune landscape in acute kidney injury prediction.Renal failure · 2025Article
- Mitochondria as a Disease-Relevant Organelle in Rheumatoid Arthritis: A Key Breakout in Fight Against the Disease.Biomedicines · 2025Review
- Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.Antioxidants (Basel, Switzerland) · 2025Review
- The role of hypoxic microenvironment in rheumatoid arthritis.Frontiers in immunology · 2025Review
- The Role of Mitochondrial Regulation in Macrophage Polarization: Implications for the Pathogenesis of Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Metabolic reprogramming: the central mechanism driving inflammatory polarization in rheumatoid arthritis and the regulatory role of traditional Chinese medicine.Frontiers in immunology · 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is an inflammatory autoimmune disease, primarily characterized by chronic symmetric synovial inflammation and erosive bone destruction.Mitochondria, the primary site of cellular energy production, play a crucial role in energy metabolism and possess homeostatic regulation capabilities. Mitochondrial function influences the differentiation, activation, and survival of both immune and non-immune cells involved in RA pathogenesis. If the organism experiences hypoxia, genetic predisposition, and oxidative stress, it leads to mitochondrial dysfunction, which further affects immune cell energy metabolism, synovial cell proliferation, apoptosis, and inflammatory signaling, causing the onset and progression of RA; and, mitochondrial regulation is becoming increasingly important in the treatment of RA.In this review, we examine the structure and function of mitochondria, analyze the potential causes of mitochondrial dysfunction in RA, and focus on the mechanisms by which mitochondrial dysfunction triggers chronic inflammation and immune disorders in RA. We also explore the effects of mitochondrial dysfunction on RA immune cells and osteoblasts, emphasizing its key role in the immune response and inflammatory processes in RA. Furthermore, we discuss potential biological processes that regulate mitochondrial homeostasis, which are of great importance for the prevention and treatment 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.