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September 10, 2025Frontiers in ImmunologyOpen Access

Myeloid-specific S100A8/A9 deficiency attenuates atrial fibrillation through prevention of TLR4/NF-kB-mediated immune cell recruitment and inflammation

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Authors

QWQing WangHSHua ShenJWJing Wang

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Overview

Conditional knockout of S100A9 decreases inflammation and AF severity, suggesting TLR4/NF-kB is critical.

Key Points

  • S100A9 deficiency cut AF duration and severity, indicating its role in promoting inflammation.
  • Patients with AF showed significantly increased S100A8/A9 levels and immune cell activation markers.
  • Transcriptomic analysis identified S100A8/A9 as a key player in inflammation linked to AF pathogenesis.
  • Inhibition of the TLR4/NF-kB pathway reveals a potential target for AF treatment and prevention.

Cite This Study

Wang et al. (2025) studied this question.

synapsesocial.com/papers/68c23c20b210217d647878behttps://doi.org/10.3389/fimmu.2025.1623486
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Single-cell RNA sequencing reveals that myeloid S100A8/A9 is a novel regulator of the transition from adaptive hypertrophy to heart failure after pressure overload2025
  2. 2The alarmin tandem: unraveling the complex effect of S100A8/A9 – from atherosclerosis to cardiac arrhythmias2025
  3. 3Chronic skin and systemic inflammation modulated by S100A8 and S100A9 complexes 47372025
  4. 4Critical role of niche S100A8 for acute myeloid leukemia progression and hematopoiesis regeneration2025 · 4 citations
  5. 5S100A9 promotes inflammasome-dependent autoinflammation by blocking the degradation of SYK tyrosine kinase2025