Background: The prevalence of atrial fibrillation (AF) is significantly higher in rheumatoid arthritis (RA) patients, but the underlying mechanisms remain poorly understood. The goal of this study was to assess the effects of RA on AF susceptibility and atrial arrhythmogenic remodeling in a rat model of RA.
Methods And Results: Collagen-induced arthritis was induced in rats by immunization with type II collagen in Freund's incomplete adjuvant. Among the rats that developed arthritis, AF susceptibility and atrial remodeling were examined 8 weeks after the primary immunization. AF inducibility and duration were substantially increased in collagen-induced arthritis rats, and AF duration was significantly and positively correlated with the serum IL-6 and TNF-α levels. Rats with collagen-induced arthritis showed prolonged atrial conduction time with no changes in the atrial effective refractory period. Atrial conduction delay was accompanied by significantly increased atrial fibrosis. In addition, atrial structural and autonomic remodeling, including left atrial dilation, apoptosis and autophagy of atrial myocytes, and atrial heterogeneous sympathetic hyperinnervation, was observed. Interestingly, we found that collagen-induced arthritis had no significant effects on connexins, Nav1.5, and the main ion channels' protein expressions in atria.
Conclusions: We demonstrated that RA increased AF susceptibility by inducing AF-promoting atrial remodeling. This study may provide insights into mechanisms underlying RA-induced AF and validate a model that is suitable for further mechanistic and therapeutic exploration.
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http://dx.doi.org/10.1161/JAHA.117.007320 | DOI Listing |
Pharmacol Res
January 2025
University Hospital of Jena, Institute of Physiology 1, D-07740 Jena, Germany. Electronic address:
Musculoskeletal pain has a high prevalence of transition to chronic pain and/or persistence as chronic pain for years or even a lifetime. Possible mechanisms for the development of such pain states are often reflected in inflammatory or neuropathic processes involving, among others, cytokines and other molecules. Since biologics such as blockers of TNF or IL-6 can attenuate inflammation and pain in a subset of patients with rheumatoid arthritis, the question arises to what extent cytokines are involved in the generation of pain in human musculoskeletal diseases.
View Article and Find Full Text PDFPublic Health Nurs
January 2025
Symbiosis College of Nursing, Symbiosis International (Deemed University), Pune, India.
Background: Subclinical vitamin D insufficiency is frequent in both developing and developed countries. Even after rickets was eliminated in the 1930s by fortifying milk, up to 1 billion people worldwide suffer from subclinical vitamin D deficiency (VDD). Numerous noncommunicable diseases (NCDs), including depression, autoimmune illnesses, diabetes, osteoporosis, and cardiovascular disease, are linked to this deficiency.
View Article and Find Full Text PDFEquine Vet J
January 2025
Department of Veterinary Clinical Sciences, University of Copenhagen, Taastrup, Denmark.
Background: MicroRNAs, a class of small noncoding RNAs, serve as post-transcriptional regulators of gene expression and are present in a stable and quantifiable form in biological fluids. MicroRNAs may influence intra-articular responses and the course of disease, but very little is known about their temporal changes in osteoarthritis.
Objectives: To identify miRNAs and characterise the temporal changes in their abundance in SF from horses with experimentally induced osteoarthritis.
Clin Rheumatol
January 2025
Department of Rheumatology and Immunology, Arthritis Research Institute, The First Affiliated Hospital of Anhui Medical University, Hefei, 230000, China.
Objective: Nuclear transcription factor-κB (NF-κB) activation is a pivotal event in the pathogenesis of osteoarthritis (OA). OA patients frequently exhibit vitamin D (VD) deficiency, which is commonly associated with NF-κB activation. Our study aimed to investigate whether VD could protect against OA by modulating NF-κB pathway and to explore the underlying mechanisms.
View Article and Find Full Text PDFInflamm Res
January 2025
Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, School of Pharmacy, Anhui Medical University, Hefei, 230032, Anhui Province, China.
Objective: Fibroblast-like synoviocytes (FLS) are key players in rheumatoid arthritis (RA) by resisting apoptosis via increased autophagy. Elevated synovial aquaporin 1 (AQP1) affects RA FLS behaviors, but its relationship with FLS autophagy is unclear. We aim to clarify that silencing AQP1 inhibits autophagy to exert its anti-RA effects.
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