ArticleJournal of inflammation research2021
iTRAQ and PRM-Based Proteomic Analysis Provides New Insights into Mechanisms of Response to Triple Therapy in Patients with Rheumatoid Arthritis.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 12 citations in OpenAlex.
- Proteomic and glycosylation biomarkers in rheumatoid arthritis: advancing early diagnosis and precision therapy.Clinical proteomics · 2026Review
- The HNRNPC/CELF2 signaling pathway drives glycolytic reprogramming and mitochondrial dysfunction in drug-resistant acute myeloid leukemia.Cell & bioscience · 2025Article
- Proteomic analysis reveals biomarkers associated with performance-based joint function and patient-reported outcomes in knee osteoarthritis.Osteoarthritis and cartilage open · 2025Article
- Ferroptosis in Arthritis: Driver of the Disease or Therapeutic Option?International journal of molecular sciences · 2024Review
- Current insights into the functional roles of ferroptosis in musculoskeletal diseases and therapeutic implications.Frontiers in cell and developmental biology · 2023Review
- The mechanism of the anti-inflammatory effect of Oldenlandia diffusa on arthritis model rats: a quantitative proteomic and network pharmacologic study.Annals of translational medicine · 2022Article
- -Omic Approaches and Treatment Response in Rheumatoid Arthritis.Pharmaceutics · 2022Review
- Ferroptosis in inflammatory arthritis: A promising future.Frontiers in immunology · 2022Review
- Ferroptosis and musculoskeletal diseases: "Iron Maiden" cell death may be a promising therapeutic target.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundApproximately 30% of patients with rheumatoid arthritis (RA) respond poorly to combination therapy of multiple drugs. The molecular mechanisms of different responses to methotrexate + leflunomide + infliximab therapy in patients with RA were explored in this study.
methodsInfliximab was administered to patients with RA whose disease activity score was higher than 5.1 after 1 month of combination therapy with methotrexate and leflunomide. After 14 weeks of undergoing triple therapy, patients with RA were classified as responders and non-responders. Protein profiles at baseline and 14th week were investigated via isobaric tags for relative and absolute quantification (iTRAQ), and proteins with significant differences ≥1.2 folds change or ≤0.8 folds change were defined as differentially expressed proteins (DEPs). Overlapping DEPs between responders and non-responders were confirmed by parallel reaction monitoring (PRM). Bioinformatic analyses were performed for DEPs.
resultsThe results revealed 5 non-responders (NRs) and 15 responders (Rs). iTRAQ analysis indicated 13 overlapping DEPs and included 6 opposite change DEPs such as testicular tissue protein Li 70, cofilin 1, fibrinogen beta chain, galectin-10, serotransferrin (TF) and albumin. The difference in serotransferrin between responders and non-responders confirmed by PRM was significant. Verification by PRM indicated that TF was elevated in the Rs group and was reduced in the NRs group. Bioinformatic analysis indicated that serotransferrin was involved in the hypoxia-inducible factor-1 pathway and ferroptosis.
conclusionSerotransferrin-related molecular mechanism may be a new direction to study refractory RA.
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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 Socratic graph.