ArticleInternational journal of molecular sciences2026
Serum Amyloid A-Dependent Inflammasome Activation and Acute Injury in a Mouse Model of Experimental Stroke.
Article in International journal of molecular sciences, 2026. 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.
- Exerkine-Mediated Regulation of the NLRP3 Inflammasome in Neuroprotection: Mechanistic Insights and the Role of Exercise.Molecular neurobiology · 2026Review
- Role of serum amyloid A in Mycoplasma pneumoniae pneumonia and related respiratory diseases.Frontiers in pediatrics · 2026Review
- Targeting SAA expression via siRNA mitigates preterm birth induced by maternal inflammation.Frontiers in pharmacology · 2026Article
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
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7 authors.
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Abstract
Serum amyloid A (SAA) proteins increase significantly in the blood following inflammation. Recently, SAAs were increased in humans following stroke and in ischemic animal models. However, the impact of SAAs on whether this signal is critical in the ischemic brain remains unknown. Therefore, we investigated the role of SAA and SAA signaling in the ischemic brain. Wild-type and SAA-deficient mice were exposed to middle cerebral artery occlusion and reperfusion and examined to determine the impact of infarct volumes, behavioral changes, inflammatory markers, TUNEL staining, and BBB changes. The underlying mechanisms were investigated using SAA-deficient mice, transgenic mice, and viral vectors. SAA levels were significantly increased following MCAo, and mice deficient in SAA showed reduced infarct volumes and improved behavioral outcomes. SAA-deficient mice showed a reduction in TUNEL staining, inflammation, and decreased glial activation. Mice lacking acute phase SAAs demonstrated a reduction in the expression of the NLRP3 inflammasome, and SAA/NLRP3 KO mice showed improvement. The restoration of SAA expression via SAA tg mice or adenoviral expression re-established the detrimental effects of SAA. A reduction in BBB permeability was seen in SAA KO mice, and anti-SAA antibody treatment reduced the effects on ischemic injury. SAA signaling plays a critical role in regulating NLRP3-induced inflammation and glial activation in the ischemic brain. Blocking this signal will be a promising approach for treating ischemic stroke.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.