ArticleMedicine2018
High mobility group box 1 was associated with thrombosis in patients with atrial fibrillation.
Article in Medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Immune responses and activity of inflammatory mediators in pulmonary vein arrhythmogenesis.International journal of cardiology. Cardiovascular risk and prevention · 2025Review
- Elevated Serum HMGB1 Levels and Their Association with Stroke Risk of Paroxysmal Atrial Fibrillation.Journal of inflammation research · 2025Article
- Inflammation pathways as therapeutic targets in angiotensin II induced atrial fibrillation.Frontiers in pharmacology · 2025Review
- Alarmins as a Possible Target of Future Therapies for Atrial Fibrillation.International journal of molecular sciences · 2022Review
- Gegen Qinlian pills alleviate carrageenan-induced thrombosis in mice model by regulating the HMGB1/NF-κB/NLRP3 signaling.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2022Article
- Role of Inflammation in the Pathogenesis of Atrial Fibrillation.Frontiers in physiology · 2022Review
- Electroimmunology and cardiac arrhythmia.Nature reviews. Cardiology · 2021Review
- Hyperactivated RAGE in Comorbidities as a Risk Factor for Severe COVID-19-The Role of RAGE-RAS Crosstalk.Biomolecules · 2021Review
- Inflammasomes and Proteostasis Novel Molecular Mechanisms Associated With Atrial Fibrillation.Circulation research · 2020Review
- Role of inflammatory signaling in atrial fibrillation.International journal of cardiology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionHigh mobility group box 1 (HMGB1) is a member of the HMGB family that is involved in inflammatory disease-related thrombosis. We hypothesize that HMGB1 and its downstream factors are associated with thrombosis in atrial fibrillation (AF). MATERIALS AND
methodsOur experimental materials were the left atrial appendage (LAA) tissues from patients undergoing valve replacement. The samples were divided into 3 groups: a sinus rhythm group (n = 15), an AF(+)thrombus(-)group (n = 15), and an AF(+) thrombus (+)group (n = 15). The expression of HMGB1, Toll-like receptor 4 (TLR4), advanced glycation end product (RAGE), myeloid differentiation factor 88 (MyD88), nuclear factor κB (NFκB), p-NFκB, and tissue factor (TF) were detected by Western blot and immunohistochemical (IHC) staining. The expressions of interleukin-1 beta, interleukin 6, and tumor necrosis factor-alpha were detected by quantitative real-time PCR.
resultsThe Western blots revealed significantly higher expressions of HMGB1, MyD88, p-NFκB/NFκB, and TF in the AF(+)thrombus(+) group than in the other 2 groups. However, no differences in TLR4 or RAGE expression were found between the groups. IHC staining also revealed higher expressions of HMGB1 and TF in the AF(+)thrombus(+) group. The increased mRNA expressions of classic inflammatory factors (i.e., interleukin-1 beta, interleukin 6, and tumor necrosis factor-alpha) in AF(+)thrombus(+) group further validated the correlation between inflammation and thrombi in atrial fibrillation.
conclusionsHMGB1 was associated with thrombosis in patients with AF via the MyD88/NFκB pathway after adjustment for cardiac and extra cardiac inflammation variables.
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