ReviewMolecular biology reports2025
Deciphering the role of ERK and PI3K/Akt as crosstalk pathways between fibroblast-like synoviocytes and osteoclasts; novel therapeutic approach for rheumatoid arthritis.
Review in Molecular biology reports, 2025. 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
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
3 citing papers in PubMed.
- Fraxin Attenuates Rheumatoid Arthritis by Regulating Macrophage Polarization and Inhibiting Fibroblast-like Synoviocyte Proliferation.International journal of molecular sciences · 2026Article
- RNF152-mediated, ubiquitin-dependent degradation of HSP27 activates the PI3K/AKT pathway, driving synovial inflammatory cascades in TMJOA.Arthritis research & therapy · 2025Article
- Function of p53 in angiogenesis and oxidative stress in rheumatoid arthritis.Clinical and experimental medicine · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a systemic immune-mediated synovial disorder characterized by chronic inflammation in the joints, resulting in heightened bone resorption and physical disabilities. RA develops through a complex interaction of different cellular and molecular factors. Fibroblast-like synoviocytes (FLSs), which have a significant role in the pathophysiology of RA, exhibiting an aggressive and inflammatory phenotype that leads to increased osteoclastogenesis and joint destruction. Understanding the cell-to-cell communication between osteoclasts and FLSs is essential for elucidating the pathophysiology of RA and identifying potential therapeutic targets for retrieving joint integrity and function. In this review, by studying the interactions of FLS and osteoclast in the inflammatory process of the disease, the ERK and PI3K/Akt pathways were found as common points in the activation of FLSs and osteoclastogenesis, which can be introduced as potential therapeutic targets in the experimental researches aimed at reducing bone destruction.
Indexed as
Identifiers
40591034What 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.