ReviewFrontiers in physiology2019
Contributions of Animal Models to the Mechanisms and Therapies of Transthyretin Amyloidosis.
Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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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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.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Application of Omics Analysis in the Clinical Practice and Research of Transthyretin Amyloidosis.Genes · 2026Review
- CRISPR-Cas3-based editing for targeted deletions in a mouse model of transthyretin amyloidosis.Nature biotechnology · 2026Article
- Human-Induced Pluripotent Stem Cell Models for Amyloid Cardiomyopathy: From Mechanistic Insights to Therapeutic Discovery.Journal of cardiovascular development and disease · 2025Review
- Management of Hereditary Transthyretin Amyloidosis (ATTRv) Patients and Asymptomatic Carriers in Spain: The EMPATIa Study.Journal of clinical medicine · 2024Article
- A description of variant transthyretin amyloidosis (ATTRv) stage 1 patients and asymptomatic carriers in Spain: the EMPATIa study.Orphanet journal of rare diseases · 2024Article
- Enhancing RNA inhibitory activity using clamp-G-modified nucleobases.Cell reports. Physical science · 2024Article
- Multi-organ structural homogeneity of amyloid fibrils in ATTRv-T60A amyloidosis patients, revealed by Cryo-EM.bioRxiv : the preprint server for biology · 2024Article
- Emerging Therapies for Transthyretin Amyloidosis.Current oncology reports · 2023Review
- The worldwide need for amyloid diagnosis in animals.Journal of biosciences · 2023Article
- Transthyretin deposition alters cardiomyocyte sarcomeric architecture, calcium transients, and contractile force.Physiological reports · 2022Article
- Plasmin activity promotes amyloid deposition in a transgenic model of human transthyretin amyloidosis.Nature communications · 2021Article
- FTIR Spectroscopy as a Tool to Study Age-Related Changes in Cardiac and Skeletal Muscle of Female C57BL/6J Mice.Molecules (Basel, Switzerland) · 2021Article
- Transthyretin amyloid fibrils alter primary fibroblast structure, function, and inflammatory gene expression.American journal of physiology. Heart and circulatory physiology · 2021Article
- The neuropathy in hereditary transthyretin amyloidosis: A narrative review.Journal of the peripheral nervous system : JPNS · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transthyretin amyloidosis (ATTR amyloidosis) is a fatal systemic disease caused by amyloid deposits of misfolded transthyretin, leading to familial amyloid polyneuropathy and/or cardiomyopathy, or a rare oculoleptomeningeal amyloidosis. A good model system that mimic the disease phenotype is crucial for the development of drugs and treatments for this devastating degenerative disorder. The present models using fruit flies, worms, rodents, non-human primates and induced pluripotent stem cells have helped researchers understand important disease-related mechanisms and test potential therapeutic options. However, the challenge of creating an ideal model still looms, for these models did not recapitulates all symptoms, particularly neurological presentation, of ATTR amyloidosis. Recently, knock-in techniques was used to generate two humanized ATTR mouse models, leading to amyloid deposition in the nerves and neuropathic manifestation in these models. This review gives a recent update on the milestone, progress, and challenges in developing different models for ATTR amyloidosis research.
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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.