ReviewBiochemistry and biophysics reports2025
The genetic puzzle of rheumatoid arthritis: Causes, progression, and treatment.
Review in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Impact of IL6 and IL18 Promoter Polymorphisms on Circulating Cytokine Levels, Gene Expression, and Susceptibility to Rheumatoid Arthritis.International journal of molecular sciences · 2026Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a multifaceted autoimmune disorder characterized by chronic inflammation and progressive joint destruction, influenced by a complex interplay of genetic and environmental factors. Substantial evidence highlights a significant genetic contribution to RA pathogenesis, with key genetic risk factors including human leukocyte antigen (HLA) genes and non-HLA variants. These genetic elements are intricately involved in immune dysregulation, antigen presentation, and signaling pathways. The genetic heterogeneity of RA is further accentuated by gene-gene and gene-environment interactions, while biomarkers and genetic profiles associated with disease progression and joint damage continue to be rigorously explored. Additionally, the evolving field of pharmacogenomics sheds light on the challenges and prospects of developing personalized therapeutic approaches for RA. Genetic markers are being explored to predict response to various RA therapies, including DMARDs and biologics. Understanding genetic risk factors and pharmacogenomic insights can support early diagnosis, predict disease severity and progression, and improve therapeutic decisions in RA patients. The main objective of this review is to comprehensively explore current knowledge regarding the genetic factors contributing to RA susceptibility, progression, and treatment response. Furthermore, by addressing genetic risk factors, gene-environment interactions, and emerging pharmacogenomic insights, the review aims to highlight critical gaps and future directions in genetic researches related to RA.
Indexed as
Identifiers
What Socratic 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 Socratic graph.