ArticleLeukemia2020
Light chain amyloidosis induced inflammatory changes in cardiomyocytes and adipose-derived mesenchymal stromal cells.
Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Review
- Mechanisms of damage and therapies for cardiac amyloidosis: a role for inflammation?Clinical research in cardiology : official journal of the German Cardiac Society · 2026Review
- Proteomic shifts post-plasma cell therapy in AL amyloid plaques and potential implications for light chaindirected anti-fibril monoclonal antibodies.Haematologica · 2026Article
- Prognostic Value of Baseline and Soluble ST2 Change in Patients With Light Chain Cardiac Amyloidosis.Journal of the American Heart Association · 2025Article
- Amyloid Light Chain Proteins in Cardiovascular Disease: Pathogenesis and Emerging Therapies for Cardiac Amyloidosis.Pharmaceutical research · 2025Review
- In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls, and potential.Cardiovascular research · 2025Review
- Evaluation of Cytokine Levels in Cardiac Transthyretin and Immunoglobulin Light Chain Amyloidosis and Their Correlation with Myocardial Inflammatory Cells and MACE.Biomedicines · 2025Article
- The molecular landscape of AL amyloidosis.British journal of haematology · 2025Review
- Prophylactic implantation of cardioverter-defibrillator in patients with advanced light-chain amyloidosis-A pilot study.Journal of arrhythmia · 2025Article
- Whole tissue proteomic analyses of cardiac ATTR and AL unveil mechanisms of tissue damage.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2025Article
- The Prognostic Value of Platelet-to-Lymphocyte Ratio and Tricuspid Regurgitation Velocity in Patients with Light-Chain Myocardial Amyloidosis.Journal of inflammation research · 2025Article
- Cardiac Amyloidosis: State-of-the-Art Review in Molecular Pathology.Current issues in molecular biology · 2024Review
- A proteomic atlas of kidney amyloidosis provides insights into disease pathogenesis.Kidney international · 2024Article
- Examining the Difficulties in Identifying and Handling Cardiac Amyloidosis; Acquiring Important Knowledge and Robust Treatment Methods.Cardiovascular & hematological disorders drug targets · 2024Review
- Inflammation across the spectrum of hypertrophic cardiac phenotypes.Heart failure reviews · 2023Review
- Prognostic value of soluble ST2 in AL and TTR cardiac amyloidosis: a multicenter study.Frontiers in cardiovascular medicine · 2023Article
- 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
- Dissecting the Molecular Features of Systemic Light Chain (AL) Amyloidosis: Contributions from Proteomics.Medicina (Kaunas, Lithuania) · 2021Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Light chain (AL) amyloidosis is a progressive, degenerative disease characterized by the misfolding and amyloid deposition of immunoglobulin light chain (LC). The amyloid deposits lead to organ failure and death. Our laboratory is specifically interested in cardiac involvement of AL amyloidosis. We have previously shown that the fibrillar aggregates of LC proteins can be cytotoxic and arrest the growth of human RFP-AC16 cardiomyocytes in vitro. We showed that adipose-derived mesenchymal stromal cells (AMSC) can rescue the cardiomyocytes from the fibril-induced growth arrest through contact-dependent mechanisms. In this study, we examined the transcriptome changes of human cardiomyocytes and AMSC in the presence of AL amyloid fibrils. The presence of fibrils causes a 'priming' immune response in AMSC associated with interferon associated genes. Exposure to AL fibrils induced changes in the pathways associated with immune response and extracellular matrix components in cardiomyocytes. We also observed upregulation of innate immune-associated transcripts (chemokines, cytokines, and complement), suggesting that amyloid fibrils initiate an innate immune response on these cells, possibly due to phenotypic transformation. This study corroborates and expands our previous studies and identifies potential new immunologic mechanisms of action for fibril toxicity on human cardiomyocytes and AMSC rescue effect on cardiomyocytes.
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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.