The State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, People's Republic of China. Electronic address:
Published: June 2021
AI Article Synopsis
Article Abstract
Rheumatoid arthritis (RA) is the most common inflammatory arthropathy, with evidence pointing to an immune-mediated etiology that propagates chronic inflammation. Although targeted immune therapeutics and aggressive treatment strategies have substantially improved, a complete understanding of the associated pathological mechanisms of the disease remains elusive. This study aimed at investigating whether regulator of G protein signaling 10 (RGS10) could affect rheumatoid arthritis (RA) pathology by regulating the immune response. A DBA/J1 mouse model of RA was established and evaluated for disease severity. RGS10 expression was inhibited by adeno-associated virus in vivo. Moreover, small interfering RNA was used to downregulate RGS10 expression in raw 264.7 cells in vitro. Results showed that RGS10 inhibition augmented RA severity, and attenuated the increase in expression of inflammatory factors. Furthermore, activated NF-κB signaling pathways were detected following RGS10 inhibition. These results revealed that RGS10 inhibition directly aggravated the RA pathological process by activating the NF-κB signaling pathway. Therefore, RGS10 is a promising novel therapeutic target for RA treatment with a potential clinical impact.
This study aimed to explore the potential causal link between genetic predisposition to various connective tissue diseases (CTDs), namely systemic lupus erythematosus (SLE), Sjögren's syndrome (SS), polymyositis (PM), dermatomyositis (DM), systemic sclerosis (SSc), mixed connective tissue disease (MCTD), and rheumatoid arthritis (RA), and the incidence of pulmonary arterial hypertension (PAH) utilizing Mendelian randomization (MR). Employing a two-sample MR approach, genetic variants associated with CTDs served as instrumental variables to investigate the exposure-outcome relationship, with GWAS data sourced from the FinnGen Biobank. Comprehensive statistical analyses, including the inverse variance weighted (IVW) method, were conducted, alongside heterogeneity, pleiotropy, and sensitivity tests to ensure the robustness and validity of findings.
Coriander (Coriandrum sativum L.) is a nutraceutically renowned annual herb from Apiaceae family and used in cuisines in different countries in different ways to enhance the tastes, flavour and nutritional values of foods. Fruit (seed) has several medicinally valuable chemical components viz.
Rheumatoid arthritis is a complex disease marked by joint pain, stiffness, swelling, and chronic synovitis, arising from the dysregulated interaction between synoviocytes and immune cells. Its unclear etiology makes finding a cure challenging. The concept of digital twins, used in engineering, can be applied to healthcare to improve diagnosis and treatment for complex diseases like rheumatoid arthritis.
Objective: Excess cholesterol loading on arterial macrophages is linked to foam cell formation, atherosclerosis and cardiovascular risk in rheumatoid arthritis (RA). However, the effect of changes in cholesterol loading on coronary plaque trajectory and the impact of RA therapies on this relationship are unknown. We investigated the association between variations in cholesterol loading capacity (CLC) over time and atherosclerosis progression.
Interstitial lung disease (ILD) associated with rheumatoid arthritis or with connective tissue diseases such as systemic sclerosis can be collectively named systemic autoimmune rheumatic disease-associated ILDs (SARD-ILDs) or rheumatic musculoskeletal disorder-associated ILDs. SARD-ILDs result in substantial morbidity and mortality, and there is a high medical need for effective therapies that target both fibrotic and inflammatory pathways in SARD-ILD. Phosphodiesterase 4 (PDE4) hydrolyses cyclic AMP, which regulates multiple pathways involved in inflammatory processes.
