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GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues.
Arthritis Res Ther
January 2025
Xin'an Medicine Research Center, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), No 2, West Zheshan Road, Wuhu, Anhui, 241000, China.
Background: Metabolism alteration is a common complication of rheumatic arthritis (RA). This work investigated the reason behind RA-caused triglyceride (TG) changes.
Methods: Fresh RA patients' whole blood was transfused into NOD-SCID mice.
Enhancing the effectiveness of immunotherapy in rheumatoid arthritis by delaying immunosenescence triggered by fibroblast-like synoviocytes.
J Orthop Surg Res
January 2025
Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou University, No. 80, Cuiyingmen, Chengguan District, Lanzhou, Gansu Province, 730030, China.
Rheumatoid arthritis (RA) is a prevalent autoimmune disorder primarily targeting the diarthrodial joints. During the progression of RA, fibroblast-like synoviocytes (FLSs) exhibit tumor-like behavior, including increased proliferation, inflammation mediation, and aggressive phenotypes, leading to bone erosion. Additionally, T cells in RA acquire pro-inflammatory characteristics, exacerbating the inflammatory environment in affected joints and associated tissues.
View Article and Find Full Text PDFPatient-Reported Fatigue Associated with Joint Histopathology in Rheumatoid Arthritis.
ACR Open Rheumatol
January 2025
Hospital for Special Surgery and Weill Cornell Medicine, New York City, New York.
Objective: Fatigue is important for patients with rheumatoid arthritis (RA) but is poorly understood. We sought to study associations of fatigue with clinical features, disease activity, and synovial histology.
Methods: Patients meeting the American College of Rheumatology/EULAR 1987 and/or 2010 RA criteria were recruited before elective total joint replacement.
Silica-mediated exacerbation of inflammatory arthritis: A novel murine model.
bioRxiv
January 2025
Department of Immunology and Microbiology, Scripps Research, La Jolla, San Diego, USA.
Objective: The mucosal origin hypothesis in rheumatoid arthritis (RA) posits that inhalant exposures, such as cigarette smoke and crystalline silica (c-silica), trigger immune responses contributing to disease onset. Despite the established risk posed by these exposures, the mechanistic link between inhalants, lung inflammation, and inflammatory arthritis remains poorly understood, partly from the lack of a suitable experimental model. As c-silica accelerates autoimmune phenotypes in lupus models and is a recognized risk factor for several autoimmune diseases, we investigated whether c-silica exposure could induce RA-like inflammatory arthritis in mice.
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Exp Mol Med
January 2025
Lab of Translational ImmunoMedicine, Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Th17 cells are activated by STAT3 factors in the nucleus, and these factors are correlated with the pathologic progression of rheumatoid arthritis (RA). Recent studies have demonstrated the presence of STAT3 in mitochondria, but its function is unclear. We investigated the novel role of mitochondrial STAT3 (mitoSTAT3) in Th17 cells and fibroblast-like synoviocytes (FLSs) and analyzed the correlation of mitoSTAT3 with RA.
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