ReviewArthritis research & therapy2005
Rheumatoid arthritis as a hyper-endoplasmic-reticulum-associated degradation disease.
Review in Arthritis research & therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 61 citations in OpenAlex.
- Overexpression of Synoviolin and miR-125a-5p, miR-19b-3p in peripheral blood of rheumatoid arthritis patients after treatment with conventional DMARDs and methylprednisolone.Clinical rheumatology · 2024Trial
- Endoplasmic reticulum stress in diseases.MedComm · 2024Review
- Casting Light on the Janus-Faced HMG-CoA Reductase Degradation Protein 1: A Comprehensive Review of Its Dualistic Impact on Apoptosis in Various Diseases.Molecular neurobiology · 2024Review
- Advances in the study of protein folding and endoplasmic reticulum-associated degradation in mammal cells.Journal of Zhejiang University. Science. B · 2024Review
- BRD3 Regulates the Inflammatory and Stress Response in Rheumatoid Arthritis Synovial Fibroblasts.Biomedicines · 2023Article
- The histone acetyl transferases CBP and p300 regulate stress response pathways in synovial fibroblasts at transcriptional and functional levels.Scientific reports · 2023Article
- Identification of potential drug targets for rheumatoid arthritis from genetic insights: a Mendelian randomization study.Journal of translational medicine · 2023Article
- Identification of copper death-associated molecular clusters and immunological profiles in rheumatoid arthritis.Frontiers in immunology · 2023Article
- PERK signaling pathway in bone metabolism: Friend or foe?Cell proliferation · 2021Review
- PERK controls bone homeostasis through the regulation of osteoclast differentiation and function.Cell death & disease · 2020Article
- The effect of heat stress on frame switch splicing of X-box binding protein 1 gene in horse.Asian-Australasian journal of animal sciences · 2019Article
- IRE1α Implications in Endoplasmic Reticulum Stress-Mediated Development and Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2018Review
- Causes and consequences of endoplasmic reticulum stress in rheumatic disease.Nature reviews. Rheumatology · 2017Review
- The E3 ligase synoviolin controls body weight and mitochondrial biogenesis through negative regulation of PGC-1β.The EMBO journal · 2015Article
- Rheumatoid Arthritis, Immunosenescence and the Hallmarks of Aging.Current aging science · 2015Review
- Endoplasmic reticulum stress as a novel mechanism in amiodarone-induced destructive thyroiditis.The Journal of clinical endocrinology and metabolism · 2015Article
- TLR dependent XBP-1 activation induces an autocrine loop in rheumatoid arthritis synoviocytes.Journal of autoimmunity · 2014Article
- Role of endoplasmic reticulum stress in rheumatoid arthritis pathogenesis.Journal of Korean medical science · 2014Review
- Flagging and docking: dual roles for N-glycans in protein quality control and cellular proteostasis.Trends in biochemical sciences · 2012Article
- A novel pathogenic role of the ER chaperone GRP78/BiP in rheumatoid arthritis.The Journal of experimental medicine · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We introduce Synoviolin as a novel pathogenic factor in rheumatoid arthritis (RA). Experimental studies indicate that this endoplasmic reticulum (ER)-resident E3 ubiquitin ligase has important functions in the ER-associated degradation (ERAD) system, an essential system for ER homeostasis. Overexpression of Synoviolin in mice causes arthropathy with synovial hyperplasia, whereas heterozygous knockdown results in increased apoptosis of synovial cells and resistance to collagen-induced arthritis in mice. On the basis of these experimental data, we propose that excess elimination of unfolded proteins (that is, 'hyper-ERAD') by overexpression of Synoviolin triggers synovial cell overgrowth and hence a worsening of RA. Further analysis of the hyper-ERAD system may permit the complex pathomechanisms of RA to be uncovered.
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.