Insights into the treatment of rheumatoid arthritis: A paradigm in medicine

Smolen, Josef S.

doi:10.1016/j.jaut.2020.102425

Cited by 46 publications

(25 citation statements)

References 125 publications

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“…RA affects approximately 1% of the world's population and disproportionally affects female population (2). RA development is a continuous, progressive, systemic pathology process and multiple autoantibodies, including rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPA), are detectable in serum before the onset or in the early stage of RA (3)(4)(5). With the gradual interaction of various immnue and fibroblast cells and cytokines, synovial tissue gradually produces chronic inflammation accompanied by bone erosion and destruction, resulting in various clinical symptoms and injuries (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

“…RA development is a continuous, progressive, systemic pathology process and multiple autoantibodies, including rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPA), are detectable in serum before the onset or in the early stage of RA (3)(4)(5). With the gradual interaction of various immnue and fibroblast cells and cytokines, synovial tissue gradually produces chronic inflammation accompanied by bone erosion and destruction, resulting in various clinical symptoms and injuries (3)(4)(5). Further, a number of organ systems can be damaged by the systemic inflammation, such as cardiac tissue, vascular system, kidneys, lung tissue, and the nervous system (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

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Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

et al. 2021

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Rheumatoid arthritis is an autoimmune disease that exhibits significant clinical heterogeneity. There are various treatments for rheumatoid arthritis, including disease-modifying anti-rheumatic drugs (DMARDs), glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), and inflammatory cytokine inhibitors (ICI), typically associated with differentiated clinical effects and characteristics. Personalized responsiveness is observed to the standard treatment due to the pathophysiological heterogeneity in rheumatoid arthritis, resulting in an overall poor prognosis. Understanding the role of individual variation in cellular and molecular mechanisms related to rheumatoid arthritis will considerably improve clinical care and patient outcomes. In this review, we discuss the source of pathophysiological heterogeneity derived from genetic, molecular, and cellular heterogeneity and their possible impact on precision medicine and personalized treatment of rheumatoid arthritis. We provide emphasized description of the heterogeneity derived from mast cells, monocyte cell, macrophage fibroblast-like synoviocytes and, interactions within immune cells and with inflammatory cytokines, as well as the potential as a new therapeutic target to develop a novel treatment approach. Finally, we summarize the latest clinical trials of treatment options for rheumatoid arthritis and provide a suggestive framework for implementing preclinical and clinical experimental results into clinical practice.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

et al. 2021

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“…As indicated by the writing, around 30-40% of RA patients [13] are not getting profited by exemplary first-line treatment which is MTX [14]. In 2019, a few significant logical advances were made in the clinical use of ML in rheumatology [15][16][17][18][19][20].…”

Section: Related Workmentioning

confidence: 99%

An Efficient CNN for Hand X-Ray Classification of Rheumatoid Arthritis

Mate

Kureshi²,

Singh

2021

Journal of Healthcare Engineering

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Hand Radiography (RA) is one of the prime tests for checking the progress of rheumatoid joint inflammation in human bone joints. Recognizing the specific phase of RA is a difficult assignment, as human abilities regularly curb the techniques for it. Convolutional neural network (CNN) is the center for hand recognition for recognizing complex examples. The human cerebrum capacities work in a high-level way, so CNN has been planned depending on organic neural-related organizations in humans for imitating its unpredictable capacities. This article accordingly presents the convolutional neural network (CNN) which has the ability to naturally gain proficiency with the qualities and anticipate the class of hand radiographs from an expansive informational collection. The reproduction of the CNN halfway layers, which depict the elements of the organization, is likewise appeared. For arrangement of the model, a dataset of 290 radiography images is utilized. The result indicates that hand X-rays are rated with an accuracy of 94.46% by the proposed methodology. Our experiments show that the network sensitivity is observed to be 0.95 and the specificity is observed to be 0.82.

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“…As a new branch of proteomics, peptidomics can be used to analyze endogenous protein fragments in body fluids and tissues ( Baggerman et al, 2005 ). Biologically active peptides could be a potential biomarker for RA diagnosis, and attenuated inflammation both in vitro and in vivo ( Roark et al, 2016 ; Smolen, 2020 ). From a perspective of peptidomics, differentially expressed peptides have been identified between RA and normal synovial tissue groups in our previous study (8).…”

Section: Introductionmentioning

confidence: 99%

p53: A Regulator of Ferroptosis Induced by Galectin-1 Derived Peptide 3 in MH7A Cells

Zhang

Chang

et al. 2022

Front. Genet.

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Backgrounds: Rheumatoid arthritis synovial fibroblasts (RASFs) are the primary cells responsible for destruction of marginal cartilage in rheumatoid arthritis (RA). G1dP3, a bioactive peptide derived from galectin-1 domain, possesses potent anti-inflammatory and anti-proliferation properties in RASFs. This study aimed to determine the effects of G1dP3 ferroptosis induction in RASFs and to further clarify the possible mechanisms.Methods: TNF-α was used to establish a RA model in MH7A cells. Cell Counting Kit-8 assays were employed to detect MH7A cell viability with different treatments. The occurrence of ferroptosis was examined by Lipid ROS assay, cellular labile iron pool measurement, reduced glutathione/oxidized glutathione activity, Gpx4 expression and transmission electron microscopy (TEM) morphology observation. Lentiviral-mediated siRNA interference was used to determine the downstream pathway.Results: G1dP3 markedly suppressed MH7A cell viability induced by TNF-α. G1dP3-treated MH7A cells presented the morphological features of ferroptosis. Moreover, G1dP3 triggered ferroptosis in MH7A cells by promoting the accumulation of lipid peroxides as well as iron deposition. Inhibition of ferroptosis alleviated G1dP3-mediated suppression of MH7A cell viability. Furthermore, G1dP3 increased p53 expression, which in turn transcriptionally suppressed SLC7A11, a key component of system Xc− essential for ferroptosis. Knockdown of p53 abrogated the ferroptotic effects of G1dP3 on MH7A cells.Conclusion: Our findings reveal that the bioactive peptide G1dP3 promotes RASFs ferroptosis cell death via a p53/SLC7A11 axis-dependent mechanism, suggesting its potential role in the treatment of RA.

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Insights into the treatment of rheumatoid arthritis: A paradigm in medicine

Cited by 46 publications

References 125 publications

Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

An Efficient CNN for Hand X-Ray Classification of Rheumatoid Arthritis

p53: A Regulator of Ferroptosis Induced by Galectin-1 Derived Peptide 3 in MH7A Cells

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