ReviewMolecules (Basel, Switzerland)2021
The Ultrastructure of Tissue Damage by Amyloid Fibrils.
Review in Molecules (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- The causative role of amyloidosis in the cardiac complications of Alzheimer's disease: a comprehensive systematic review.The Journal of physiology · 2026Pooled it
- Transthyretin Amyloidosis-From Peculiar Neuropathy to a Treatable Chronic Multisystemic Disease.Genes · 2026Review
- Article
- Digging Deep into Alzheimer Disease: How Electron Microscopy Helps Elucidating Its Pathogenesis.Cellular and molecular neurobiology · 2026Review
- Bridging the Gap in AL and ATTR Cardiac Amyloidosis: Integrating Histopathology, Biomarkers, and Multimodal Imaging for Subtype-Specific Diagnosis.Reviews in cardiovascular medicine · 2026Review
- Prevalence of Autonomic Dysfunction and Correlation with Markers of Disease Severity in Cardiac Amyloidosis.Journal of clinical medicine · 2025Article
- Cathepsin B prevents cell death by fragmentation and destruction of pathological amyloid fibrils.Cell death discovery · 2025Article
- Clay-Polymer Nanocomposites Mediated Inhibition of Protein Aggregation: Possible Role in the Prevention of Proteinopathies.Protein and peptide letters · 2025Article
- Cardiac Amyloidosis: State-of-the-Art Review in Molecular Pathology.Current issues in molecular biology · 2024Review
- Anticoagulation in Atrial Fibrillation Associated With Cardiac Amyloidosis: A Narrative Review.Cureus · 2024Review
- Nerve pathology of microangiopathy and thromboinflammation in hereditary transthyretin amyloidosis.Annals of clinical and translational neurology · 2024Article
- Neuromuscular manifestations of wild type transthyretin amyloidosis: a review and single center's experience.Frontiers in cardiovascular medicine · 2024Review
- Amyloid detection and typing yield of skin biopsy in systemic amyloidosis and polyneuropathy.Annals of clinical and translational neurology · 2023Article
- Amyloidosis in the nasopharynx and larynx: a case report.The Journal of international medical research · 2022Article
- Rational Design of a Peptidomimetic Inhibitor of Gelsolin Amyloid Aggregation.International journal of molecular sciences · 2022Article
- Noninvasive Diagnostics of Renal Amyloidosis: Current State and Perspectives.International journal of molecular sciences · 2022Review
- Article
- Diagnostic and Prognostic Values of Cardiopulmonary Exercise Testing in Cardiac Amyloidosis.Frontiers in cardiovascular medicine · 2022Review
- Implementing Complementary Approaches to Shape the Mechanism of α-Synuclein Oligomerization as a Model of Amyloid Aggregation.Molecules (Basel, Switzerland) · 2021Review
- Molecular Mechanisms of Cardiac Amyloidosis.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Amyloidosis is a group of diseases that includes Alzheimer's disease, prion diseases, transthyretin (ATTR) amyloidosis, and immunoglobulin light chain (AL) amyloidosis. The mechanism of organ dysfunction resulting from amyloidosis has been a topic of debate. This review focuses on the ultrastructure of tissue damage resulting from amyloid deposition and therapeutic insights based on the pathophysiology of amyloidosis. Studies of nerve biopsy or cardiac autopsy specimens from patients with ATTR and AL amyloidoses show atrophy of cells near amyloid fibril aggregates. In addition to the stress or toxicity attributable to amyloid fibrils themselves, the toxicity of non-fibrillar states of amyloidogenic proteins, particularly oligomers, may also participate in the mechanisms of tissue damage. The obscuration of the basement and cytoplasmic membranes of cells near amyloid fibrils attributable to an affinity of components constituting these membranes to those of amyloid fibrils may also play an important role in tissue damage. Possible major therapeutic strategies based on pathophysiology of amyloidosis consist of the following: (1) reducing or preventing the production of causative proteins; (2) preventing the causative proteins from participating in the process of amyloid fibril formation; and/or (3) eliminating already-deposited amyloid fibrils. As the development of novel disease-modifying therapies such as short interfering RNA, antisense oligonucleotide, and monoclonal antibodies is remarkable, early diagnosis and appropriate selection of treatment is becoming more and more important for patients with amyloidosis.
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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.