ArticleProceedings of the National Academy of Sciences of the United States of America2013
Pathogenetic mechanisms of amyloid A amyloidosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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63 citing papers in PubMed, 117 citations in OpenAlex.
- Extraintestinal Manifestations of Inflammatory Bowel Disease: A Focus on Kidney Complications.International journal of molecular sciences · 2026Review
- [An unusual cause for kidney transplantation].Innere Medizin (Heidelberg, Germany) · 2026Article
- Pathogenesis and kidney prognosis of renal amyloidosis.Cellular and molecular life sciences : CMLS · 2026Review
- Systemic Consequences of Chronic Ethanol Intake: From Microbiome Shifts to Metabolic Impairment.Comprehensive physiology · 2026Article
- Assessment of the biochemical basis underlying the resistance against systemic amyloidosis.Scientific reports · 2026Article
- Serum amyloid A in the oral microenvironment: implications for inflammation, host-microbe interactions, and disease monitoring.Frontiers in immunology · 2026Review
- Adalimumab for AA Amyloidosis Secondary to Severe Hidradenitis Suppurativa.Case reports in nephrology · 2026Article
- Destabilization of Helix III Initiates Early Serum Amyloid A Misfolding by Exposing Its Amyloidogenic Core.The journal of physical chemistry letters · 2025Article
- What Cardiologists Should Know About Amyloidosis.Journal of clinical medicine · 2025Review
- Serum Amyloid A: A Double-Edged Sword in Health and Disease.International journal of molecular sciences · 2025Review
- Integrated Clinomics and Molecular Dynamics Simulation Approaches Reveal the SAA1.1 Allele as a Biomarker in Alkaptonuria Disease Severity.Biomolecules · 2025Article
- Identification and characterization of spontaneous AA amyloidosis in CD-1 mice used in toxicity studies: implications of SAA1 and SAA2 copy number variations.Journal of toxicologic pathology · 2025Article
- Real-Time 3D Imaging and Inhibition Analysis of Human Serum Amyloid A Aggregations Using Quantum Dots.International journal of molecular sciences · 2024Article
- Secondary amyloidosis in inflammatory bowel disease patients: findings from three tertiary medical centers.Clinical journal of gastroenterology · 2024Article
- HGA Triggers SAA Aggregation and Accelerates Fibril Formation in the C20/A4 Alkaptonuria Cell Model.Cells · 2024Article
- Assessment of health impacts in retired antisera-producing horses: Blood biochemistry and serum amyloid A analysis.Veterinary world · 2024Article
- The ASC inflammasome adapter governs SAA-derived protein aggregation in inflammatory amyloidosis.EMBO molecular medicine · 2024Article
- Interactions of Serum Amyloid A Proteins with the Blood-Brain Barrier: Implications for Central Nervous System Disease.International journal of molecular sciences · 2024Review
- Anakinra-Associated Systemic Amyloidosis.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- Deficiency of Acute-Phase Serum Amyloid A Exacerbates Sepsis-Induced Mortality and Lung Injury in Mice.International journal of molecular sciences · 2023Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 1 institution in 2 countries.
Funding
Abstract
Systemic amyloid A (AA) amyloidosis is a serious complication of chronic inflammation. Serum AA protein (SAA), an acute phase plasma protein, is deposited extracellularly as insoluble amyloid fibrils that damage tissue structure and function. Clinical AA amyloidosis is typically preceded by many years of active inflammation before presenting, most commonly with renal involvement. Using dose-dependent, doxycycline-inducible transgenic expression of SAA in mice, we show that AA amyloid deposition can occur independently of inflammation and that the time before amyloid deposition is determined by the circulating SAA concentration. High level SAA expression induced amyloidosis in all mice after a short, slightly variable delay. SAA was rapidly incorporated into amyloid, acutely reducing circulating SAA concentrations by up to 90%. Prolonged modest SAA overexpression occasionally produced amyloidosis after long delays and primed most mice for explosive amyloidosis when SAA production subsequently increased. Endogenous priming and bulk amyloid deposition are thus separable events, each sensitive to plasma SAA concentration. Amyloid deposits slowly regressed with restoration of normal SAA production after doxycycline withdrawal. Reinduction of SAA overproduction revealed that, following amyloid regression, all mice were primed, especially for rapid glomerular amyloid deposition leading to renal failure, closely resembling the rapid onset of renal failure in clinical AA amyloidosis following acute exacerbation of inflammation. Clinical AA amyloidosis rarely involves the heart, but amyloidotic SAA transgenic mice consistently had minor cardiac amyloid deposits, enabling us to extend to the heart the demonstrable efficacy of our unique antibody therapy for elimination of visceral amyloid.
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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.