ArticleThe American journal of pathology2015
Hepatic expression of serum amyloid A1 is induced by traumatic brain injury and modulated by telmisartan.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 41 citations in OpenAlex.
- Intranasal CRISPR lipid nanoparticles targeting MAPK9 attenuate neuroinflammation after traumatic brain injury.Biomedical microdevices · 2026Article
- Intranasal CRISPR- lipid nanoparticles targeting MAPK9 reduce neuroinflammation after traumatic brain injury.Research square · 2026Article
- Intranasal CRISPR-lipid nanoparticles targeting MAPK9 reduce neuroinflammation after traumatic brain injury.bioRxiv : the preprint server for biology · 2026Article
- Remission of severe familial proteinuria in a Bracco Italiano dog.The Canadian veterinary journal = La revue veterinaire canadienne · 2026Article
- Prediction of influenza virus infection based on deep learning and peripheral blood proteomics: A diagnostic study.Journal of advanced research · 2026Article
- Modulatory Role of Arbutin on Hepatic Inflammation and Apoptosis After Mild Repetitive Traumatic Brain Injury in Experimental Rats: Involvement of NGF/TrkA and IL-6/JAK2/STAT3 Immune Signaling Crosstalk.Biochemistry research international · 2026Article
- Placenta-Derived Secretions Promote Liver Dysfunction, and Hepatic Serum Amyloid A Mediates Kidney Inflammatory Response in a Preeclampsia-like Mouse Model.International journal of molecular sciences · 2025Article
- The application of telmisartan in central nervous system disorders.Pharmacological reports : PR · 2025Review
- Development of a Genetically Modified Lactococcus lactis Strain that Produces a Single-Chain Variable Fragment Targeting Interleukin-6 Receptor α to Suppress Serum Amyloid A.Current microbiology · 2025Article
- Recent Advances in Studies of Serum Amyloid A: Implications in Inflammation, Immunity and Tumor Metastasis.International journal of molecular sciences · 2025Review
- Identification of a risk model for prognostic and therapeutic prediction in renal cell carcinoma based on infiltrating M0 cells.Scientific reports · 2024Article
- Liver fibrosis score is associated with the mortality of traumatic brain injury patients.Neurosurgical review · 2023Article
- Serum amyloid A and metabolic disease: evidence for a critical role in chronic inflammatory conditions.Frontiers in cardiovascular medicine · 2023Review
- Fecal Microbiota Transplantation Derived from Alzheimer's Disease Mice Worsens Brain Trauma Outcomes in Wild-Type Controls.International journal of molecular sciences · 2022Article
- Utility of serum amyloid A as a potential prognostic biomarker of aneurysmal subarachnoid hemorrhage.Frontiers in neurology · 2022Article
- Fast Maturation of Splenic Dendritic Cells Upon TBI Is Associated With FLT3/FLT3L Signaling.Frontiers in immunology · 2022Article
- SAA1 Expression as a Potential Prognostic Marker of the Tumor Microenvironment in Glioblastoma.Frontiers in neurology · 2022Article
- Biomimetic Nanoparticles as a Theranostic Tool for Traumatic Brain Injury.Advanced functional materials · 2021Article
- Bidirectional Brain-Systemic Interactions and Outcomes After TBI.Trends in neurosciences · 2021Review
- The interaction between brain and liver regulates lipid metabolism in the TBI pathology.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Traumatic brain injury affects the whole body in addition to the direct impact on the brain. The systemic response to trauma is associated with the hepatic acute-phase response. To further characterize this response, we performed controlled cortical impact injury on male mice and determined the expression of serum amyloid A1 (SAA1), an apolipoprotein, induced at the early stages of the acute-phase response in liver and plasma. After cortical impact injury, induction of SAA1 was detectable in plasma at 6 hours post-injury and in liver at 1 day post-injury, followed by gradual diminution over time. In the liver, cortical impact injury increased neutrophil and macrophage infiltration, apoptosis, and expression of mRNA encoding the chemokines CXCL1 and CXCL10. An increase in angiotensin II AT1 receptor mRNA at 3 days post-injury was also observed. Administration of the AT1 receptor antagonist telmisartan 1 hour post-injury significantly decreased liver SAA1 levels and CXCL10 mRNA expression, but did not affect CXCL1 expression or the number of apoptotic cells or infiltrating leukocytes. To our knowledge, this is the first study to demonstrate that SAA1 is induced in the liver after traumatic brain injury and that telmisartan prevents this response. Elucidating the molecular pathogenesis of the liver after brain injury will assist in understanding the efficacy of therapeutic approaches to brain injury.
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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 OpenQuestion graph.