ArticleThe Journal of biological chemistry2018
Plasminogen activation triggers transthyretin amyloidogenesis
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Redefining the epidemiology of cardiac amyloidosis. A systematic review and meta-analysis of screening studies.European journal of heart failure · 2022Pooled it
- Do Extracellular Vesicles and the Biochemical Microenvironment Contribute to Amyloid Transthyretin Cardiomyopathy?JACC. Advances · 2026Article
- Quantitative Proteomics of Plasma-Derived Extracellular Vesicles Reveals a Plasminogen-Centered Protein Network in Transthyretin Cardiac Amyloidosis.JACC. Advances · 2026Article
- Pathogenesis and kidney prognosis of renal amyloidosis.Cellular and molecular life sciences : CMLS · 2026Review
- Transthyretin is a novel innate immune effector against Gram negative bacteria.PLoS pathogens · 2026Article
- Association Between Occupational Physical Work Exposure and Wild-Type Transthyretin Cardiomyopathy.JACC. Advances · 2026Article
- 3D Visualization and Proteomic Analysis of Human Cardiac Transthyretin Amyloidosis Tissue Reveals Microangiopathy and Capillary Occlusion.bioRxiv : the preprint server for biology · 2026Article
- Human-Induced Pluripotent Stem Cell Models for Amyloid Cardiomyopathy: From Mechanistic Insights to Therapeutic Discovery.Journal of cardiovascular development and disease · 2025Review
- In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls, and potential.Cardiovascular research · 2025Review
- A Tale of Two Diseases: Decoding Aortic Stenosis and Cardiac Amyloidosis.Journal of clinical medicine · 2025Review
- Initiation of transthyretin aggregation at neutral pH by fluid agitation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Evolving Strategies in Cardiac Amyloidosis: From Mechanistic Discoveries to Diagnostic and Therapeutic Advances.Cardiology clinics · 2025Review
- Wild-type transthyretin cardiac amyloidosis and aortic stenosis: Can carpal tunnel syndrome help distinguish the chicken from the egg?Journal of internal medicine · 2025Article
- Knowledge Landscape and Hotspots of Research in Transthyretin Amyloid Cardiomyopathy: A Bibliometric Analysis.International journal of medical sciences · 2025Article
- Amyloids and the Heart: An Update.Journal of clinical medicine · 2024Review
- Aggregation of Transthyretin by Fluid Agitation.bioRxiv : the preprint server for biology · 2024Article
- A Snapshot of the Most Recent Transthyretin Stabilizers.International journal of molecular sciences · 2024Review
- Identification of the interfacial regions in misfolded transthyretin oligomers.Biochimica et biophysica acta. Proteins and proteomics · 2024Article
- Degradation versus fibrillogenesis, two alternative pathways modulated by seeds and glycosaminoglycans.Protein science : a publication of the Protein Society · 2024Article
- Amyposomes, a nanotechnological chaperone with anti-amyloidogenic activity.Annals of medicine · 2023Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 3 countries.
Funding
Abstract
Systemic amyloidosis is a usually fatal disease caused by extracellular accumulation of abnormal protein fibers, amyloid fibrils, derived by misfolding and aggregation of soluble globular plasma protein precursors. Both WT and genetic variants of the normal plasma protein transthyretin (TTR) form amyloid, but neither the misfolding leading to fibrillogenesis nor the anatomical localization of TTR amyloid deposition are understood. We have previously shown that, under physiological conditions, trypsin cleaves human TTR in a mechano-enzymatic mechanism that generates abundant amyloid fibrils
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What OpenQuestion holds
Registered trials
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.