ArticleAmerican journal of physiology. Heart and circulatory physiology2019
Zebrafish model of amyloid light chain cardiotoxicity: regeneration versus degeneration.
Article in American journal of physiology. Heart and circulatory physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
20 citing papers in PubMed, 30 citations in OpenAlex.
- Changes in Myocardial Light Chain Amyloid Burden After Plasma Cell Therapy.JACC. Cardiovascular imaging · 2025Trial
- Mechanisms of damage and therapies for cardiac amyloidosis: a role for inflammation?Clinical research in cardiology : official journal of the German Cardiac Society · 2026Review
- Central nervous system involvement in cardiac amyloidosis: Redefining the heart-brain axis.European journal of clinical investigation · 2026Review
- In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls, and potential.Cardiovascular research · 2025Review
- Modeling immunoglobulin light chain amyloidosis in Caenorhabditis elegans.Disease models & mechanisms · 2025Article
- Amyloidogenic immunoglobulin light chains disturb contractile function and calcium transients in a human cardiac spheroid model of light chain (AL) amyloidosis.Scientific reports · 2025Article
- Cardio-Hepatic Interaction in Cardiac Amyloidosis.Journal of clinical medicine · 2024Article
- Amyloidogenic light chains impair plasma cell survival.Haematologica · 2023Article
- Role of the mechanisms for antibody repertoire diversification in monoclonal light chain deposition disorders: when a friend becomes foe.Frontiers in immunology · 2023Review
- Molecular Mechanism of Pathogenesis and Treatment Strategies for AL Amyloidosis.International journal of molecular sciences · 2022Review
- Understanding AL amyloidosis with a little help fromFrontiers in immunology · 2022Review
- Article
- Dissecting the Molecular Features of Systemic Light Chain (AL) Amyloidosis: Contributions from Proteomics.Medicina (Kaunas, Lithuania) · 2021Review
- Preclinical Models of Cancer Therapy-Associated Cardiovascular Toxicity: A Scientific Statement From the American Heart Association.Circulation research · 2021Review
- Prognostic implications of pericardial and pleural effusion in patients with cardiac amyloidosis.Clinical research in cardiology : official journal of the German Cardiac Society · 2021Article
- Future Perspectives.Hematology/oncology clinics of North America · 2020Review
- Review
- Autophagy Activation in Zebrafish Heart Regeneration.Scientific reports · 2020Article
- Harnessing Cardiac Regeneration as a Potential Therapeutic Strategy for AL Cardiac Amyloidosis.Current cardiology reports · 2020Review
- Amyloidosis in Heart Failure.Current heart failure reports · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Cardiac dysfunction is the most frequent cause of morbidity and mortality in amyloid light chain (AL) amyloidosis caused by a clonal immunoglobulin light chain (LC). Previously published transgenic animal models of AL amyloidosis have not recapitulated the key phenotype of cardiac dysfunction seen in AL amyloidosis, which has limited our understanding of the disease mechanisms in vivo, as well as the development of targeted AL therapeutics. We have developed a transgenic zebrafish model in which a λ LC derived from a patient with AL amyloidosis is conditionally expressed in the liver under the control of the Gal4 upstream activation sequence enhancer system. Circulating LC levels of 125 µg/ml in these transgenic zebrafish are comparable to median pathological serum LC levels. Functional analysis links abnormal contractile function with evidence of cellular and molecular proteotoxicity in the heart, including increased cell death and autophagy. However, despite pathological and functional phenotypes analogous to human AL, the lifespan of the transgenic fish is comparable to control fish without the expressed AL-LC transgene. Nuclear labeling experiments suggest increased cardiac proliferation in the transgenic fish, which can be counteracted by treatment with a small molecule proliferation inhibitor leading to increased zebrafish mortality because of cardiac apoptosis and functional deterioration. This transgenic zebrafish model provides a platform to study underlying AL disease mechanisms in vivo further.
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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.