ArticlePloS one2015
Light Chain Amyloid Fibrils Cause Metabolic Dysfunction in Human Cardiomyocytes.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
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
37 citing papers in PubMed, 70 citations in OpenAlex.
- Phase 2 trial of daily, oral epigallocatechin gallate in patients with light-chain amyloidosis.International journal of hematology · 2017Trial
- Biomolecular mechanisms of cardiac amyloidosis and its cardiovascular pathological basis.Frontiers in immunology · 2026Review
- Mitochondrial Dysfunction in Cardiomyopathy and Heart Failure: From Energetic Collapse to Therapeutic Opportunity.Biomolecules · 2025Review
- In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls, and potential.Cardiovascular research · 2025Review
- Cardiac Amyloidosis: State-of-the-Art Review in Molecular Pathology.Current issues in molecular biology · 2024Review
- Re-Engineering Therapeutic Anti-Aβ Monoclonal Antibody to Target Amyloid Light Chain.International journal of molecular sciences · 2024Article
- Mechanisms of left ventricular systolic dysfunction in light chain amyloidosis: a multiparametric cardiac MRI study.Frontiers in cardiovascular medicine · 2024Article
- Pharmacological stabilization of the native state of full-length immunoglobulin light chains to treat light chain amyloidosis.Current opinion in chemical biology · 2023Review
- Implications of Extra-cardiac Disease in Patient Selection for Heart Transplantation: Considerations in Cardiac Amyloidosis.Cardiac failure review · 2023Review
- Role of the mechanisms for antibody repertoire diversification in monoclonal light chain deposition disorders: when a friend becomes foe.Frontiers in immunology · 2023Review
- Understanding AL amyloidosis with a little help fromFrontiers in immunology · 2022Review
- Molecular Mechanisms of Cardiac Amyloidosis.International journal of molecular sciences · 2021Review
- Mechanisms and Potential Treatment Options of Heart Failure in Patients With Multiple Myeloma.Cureus · 2021Review
- Early events in light chain aggregation at physiological pH reveal new insights on assembly, stability, and aggregate dissociation.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2021Article
- Quercetin Disaggregates Prion Fibrils and Decreases Fibril-Induced Cytotoxicity and Oxidative Stress.Pharmaceutics · 2020Article
- Insight from an autopsy in a patient with rapidly worsening heart failure due to amyloid light-chain cardiac amyloidosis: A case report.Journal of cardiology cases · 2020Article
- Light chain amyloidosis induced inflammatory changes in cardiomyocytes and adipose-derived mesenchymal stromal cells.Leukemia · 2020Article
- Sudden death in lambda light chain AL cardiac amyloidosis: a review of literature and update for clinicians and pathologists.International journal of clinical and experimental pathology · 2020Review
- Macrophage-Mediated Phagocytosis and Dissolution of Amyloid-Like Fibrils in Mice, Monitored by Optical Imaging.The American journal of pathology · 2019Article
- Cryo-EM structure of a light chain-derived amyloid fibril from a patient with systemic AL amyloidosis.Nature communications · 2019Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Light chain (AL) amyloidosis is the most common form of systemic amyloid disease, and cardiomyopathy is a dire consequence, resulting in an extremely poor prognosis. AL is characterized by the production of monoclonal free light chains that deposit as amyloid fibrils principally in the heart, liver, and kidneys causing organ dysfunction. We have studied the effects of amyloid fibrils, produced from recombinant λ6 light chain variable domains, on metabolic activity of human cardiomyocytes. The data indicate that fibrils at 0.1 μM, but not monomer, significantly decrease the enzymatic activity of cellular NAD(P)H-dependent oxidoreductase, without causing significant cell death. The presence of amyloid fibrils did not affect ATP levels; however, oxygen consumption was increased and reactive oxygen species were detected. Confocal fluorescence microscopy showed that fibrils bound to and remained at the cell surface with little fibril internalization. These data indicate that AL amyloid fibrils severely impair cardiomyocyte metabolism in a dose dependent manner. These data suggest that effective therapeutic intervention for these patients should include methods for removing potentially toxic amyloid fibrils.
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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.