ArticleJournal of biomedical research2011
TLR2 was overexpressed independent of IL-6 in patients with valvular atrial fibrillation.
Article in Journal of biomedical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Atrial Myopathy and Heart Failure: Immunomolecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2025Review
- Elucidating the molecular association and potential mechanisms between psoriasis and atrial fibrillation through biomarker and immune infiltration analysis.Archives of dermatological research · 2025Article
- Review
- Inflammation and the pathogenesis of atrial fibrillation.Nature reviews. Cardiology · 2015Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor 2 (TLR2) has recently been shown to be up-regulated in patients with non-valvular atrial fibrillation (AF). The present study was aimed to determine whether the pathogenesis and development of AF is associated with the up-regulation of TLR2. Clinical data and right atrial appendage (RAA) specimens were collected from 20 patients with persisten AF (PeAF), 15 patients with paroxysmal AF (PaAF) and 13 patients with no history of AF undergoing valvular replacement. The results showed that gene expression and protein content of TLR2 were increased in both the AF subgroups, compared with the sinus rhythm (SR) group. Between the two AF subgroups, PaAF had a higher TLR2 level than PeAF. However, no difference in interluekin (IL)-6 content was found among the three groups, and no correlation was found between TLR2 and IL-6 in PeAF patients (r = 0.090, P = 0.706), PaAF patients (r = 0.408, P = 0.131) and AF patients (r = -0.301, P = 0.079). Immunohistochemical analysis revealed that TLR2 was distributed in RAAs of AF patients and confirmed the immunoblotting results. In conclusion, we demonstrated that TLR2 was elevated in AF (especially PaAF) patients with valvular heart disease, further implicating inflammation involved in the pathogenesis and development of AF.
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