ArticleKidney international2020
Novel clinical manifestations and treatment of hereditary apoA-I amyloidosis: when a good protein turns bad.
Article in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
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Who cites it
5 citing papers in PubMed.
- Structural Basis for the Pro-amyloidogenic Action and Ligand Binding of a Novel W72R Variant of Human Apolipoprotein A-I.Journal of molecular biology · 2026Article
- Cryo-EM reveals structural variability of apolipoprotein A-I amyloid fibrils across organs, mutations, and clinical presentations.Nature communications · 2026Article
- Concurrence of renal amyloidosis and membranous nephropathy: a case series and literature review.BMC nephrology · 2026Review
- An unusual phenotype of hereditary AApoAI amyloidosis caused by a novel Asp20Tyr substitution is linked to pH-dependent aggregation of apolipoprotein A-I.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Physicochemical mechanisms of aggregation and fibril formation of α-synuclein and apolipoprotein A-I.Biophysics and physicobiology · 2024Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Amyloidoses are life-threatening diseases caused by the deposition of various proteins including apolipoprotein A-I, the major protein of plasma high-density lipoprotein. Timely diagnostics of amyloidoses are crucial for their treatment. Colombat et al. reported novel aspects of the hereditary apolipoprotein A-I amyloidosis, including its unexpected clinical presentation and genetic origins, as well as life- and vision-saving hepatorenal transplantation. This study improves the diagnostics of apolipoprotein A-I amyloidosis, optimizes its treatment, and expands our understanding of the molecular basis of this multipronged disease.
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