ReviewInflammopharmacology2021
Exploring the therapeutic promise of targeting Rho kinase in rheumatoid arthritis.
Review in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Systematic analysis of adverse reaction signals induced by leflunomide, upadacitinib, and baricitinib in the treatment of rheumatoid arthritis: a FAERS database analysis.Frontiers in medicine · 2026Article
- Exploring the mechanism of triptolide inhibiting the motility of fibroblast-like synoviocytes in rheumatoid arthritis via RhoA/Rho-associated kinase axis, based on network pharmacology, molecular docking and molecular dynamics simulations.Frontiers in pharmacology · 2025Article
- Proteomic profiling of extracellular vesicles in synovial fluid and plasma from Oligoarticular Juvenile Idiopathic Arthritis patients reveals novel immunopathogenic biomarkers.Frontiers in immunology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a prevalent systemic autoimmune disease caused by dysregulated inflammatory reactions, T lymphocyte invasion into the joints, and articular thickening. Immune cells, primarily tumor necrosis factor-alpha (TNF-α) and chemokines (interleukin or IL-1), which are predominantly generated by activated macrophages cells, have also been involved with the pathogenesis of rheumatoid arthritis. Rho GTPases are integral factors of biochemical cascades utilized by antigens, and also by cellular receptors, cytokines, and chemokines, to modulate inflammatory reactions, according to growing data. The Rho family is a group of G proteins that govern a variety of biological and physiological activities such as mobility, actin stress fiber production, growth, and polarity. Research suggests that the Rho A and Rho-associated coiled-coil kinase (ROCK) regulatory cascade could be essential in several autoimmune conditions, including RA. ROCK is activated in the synovial of rheumatoid arthritis patients, while the blocking of ROCK with fasudil could also decrease IL-6, TNF-α, and IL-1. This review covers current developments in understanding the overactivation of Rho enzyme activity in RA suppressed by ROCK inhibitors which can be utilized for the treatment of autoimmune disease. We offer an outline of the function of ROCK inhibitors in immune cells and discuss findings which emphasize the rising participation of this category of kinases within the pathological process of autoimmune disorders. Assuming the potential ability of ROCK as a therapeutic, we define approaches that might be used to inhibit Rho kinase activity in rheumatoid disorders.
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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.