ArticleScientific reports2017
Proteotoxicity in cardiac amyloidosis: amyloidogenic light chains affect the levels of intracellular proteins in human heart cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Cardiac Toxicity in the Treatment of Light Chain Amyloidosis: Systematic Review of Clinical Studies.Current drug safety · 2024Pooled it
- The Role of Cardiac Fibrosis and Fibroblast Activation in Amyloid Light Chain (AL) Amyloidosis.JACC. Basic to translational science · 2026Article
- Beyond the Fibrils: Fibroblasts and Fibrosis in Amyloid Light Chain Cardiomyopathy.JACC. Basic to translational science · 2026Article
- Histopathological improvement in kidney AL amyloid deposits following daratumumab-based chemotherapy and autologous peripheral blood stem cell transplantation: a case report.CEN case reports · 2026Article
- A journey through the molecular networks of endomyocardial biopsies to explore ATTR and ALiScience · 2026Article
- Mechanisms of damage and therapies for cardiac amyloidosis: a role for inflammation?Clinical research in cardiology : official journal of the German Cardiac Society · 2026Review
- Exploring the MicroRNA Landscape in Cardiac Amyloidosis: Molecular Insights and Clinical Applications.Genes · 2026Review
- Prevalence and Prognostic Significance of Restriction Versus Systolic Dysfunction in Patients With Transthyretin and Light Chain Cardiac Amyloidosis.Circulation. Heart failure · 2026Article
- Evaluating natural history and treatment response in cardiac amyloidosis: the evolving role of multimodality imaging.European heart journal. Cardiovascular Imaging · 2026Review
- Biomolecular mechanisms of cardiac amyloidosis and its cardiovascular pathological basis.Frontiers in immunology · 2026Review
- Immunoglobulin Free Light Chains as a Biomarker of Inflammation and Heart Failure in Myocarditis and Non-Inflammatory Heart Disease.Diagnostics (Basel, Switzerland) · 2025Article
- Microvascular obstruction in cardiac amyloidosis.European journal of heart failure · 2025Article
- Case report: recurrent chest pain as initial manifestation of rapidly progressing light-chain cardiac amyloidosis with microvascular infiltration-a novel red flag associated with poor outcomes.European heart journal. Case reports · 2025Article
- In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls, and potential.Cardiovascular research · 2025Review
- Echocardiographic risk stratification in light chain and transthyretin amyloidosis: a meta-analysis.European heart journal open · 2025Article
- Antibody Aggregation: A Problem Within the Biopharmaceutical Industry and Its Role in AL Amyloidosis Disease.The protein journal · 2025Review
- Functional Status and Quality of Life in Light-Chain Amyloidosis: Advanced Imaging, Longitudinal Changes, and Outcomes.JACC. Heart failure · 2024Article
- Cardiac Amyloidosis: State-of-the-Art Review in Molecular Pathology.Current issues in molecular biology · 2024Review
- miR-331-5p Affects Motility of Thyroid Cancer Cell Lines and Regulates BID Expression.Biomedicines · 2024Article
- A proteomic atlas of kidney amyloidosis provides insights into disease pathogenesis.Kidney international · 2024Article
Corrections and comments
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Authors and funding
19 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AL amyloidosis is characterized by widespread deposition of immunoglobulin light chains (LCs) as amyloid fibrils. Cardiac involvement is frequent and leads to life-threatening cardiomyopathy. Besides the tissue alteration caused by fibrils, clinical and experimental evidence indicates that cardiac damage is also caused by proteotoxicity of prefibrillar amyloidogenic species. As in other amyloidoses, the damage mechanisms at cellular level are complex and largely undefined. We have characterized the molecular changes in primary human cardiac fibroblasts (hCFs) exposed in vitro to soluble amyloidogenic cardiotoxic LCs from AL cardiomyopathy patients. To evaluate proteome alterations caused by a representative cardiotropic LC, we combined gel-based with label-free shotgun analysis and performed bioinformatics and data validation studies. To assess the generalizability of our results we explored the effects of multiple LCs on hCF viability and on levels of a subset of cellular proteins. Our results indicate that exposure of hCFs to cardiotropic LCs translates into proteome remodeling, associated with apoptosis activation and oxidative stress. The proteome alterations affect proteins involved in cytoskeletal organization, protein synthesis and quality control, mitochondrial activity and metabolism, signal transduction and molecular trafficking. These results support and expand the concept that soluble amyloidogenic cardiotropic LCs exert toxic effects on cardiac cells.
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