ArticleAmyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis2025
Whole tissue proteomic analyses of cardiac ATTR and AL unveil mechanisms of tissue damage.
Article in Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Reversing the pipeline: a 'human-first' multi-omics approach to cardiovascular discovery.Experimental & molecular medicine · 2026Review
- A journey through the molecular networks of endomyocardial biopsies to explore ATTR and ALiScience · 2026Article
- Exploring the MicroRNA Landscape in Cardiac Amyloidosis: Molecular Insights and Clinical Applications.Genes · 2026Review
- Application of Omics Analysis in the Clinical Practice and Research of Transthyretin Amyloidosis.Genes · 2026Review
- Biomolecular mechanisms of cardiac amyloidosis and its cardiovascular pathological basis.Frontiers in immunology · 2026Review
- Proteomic shifts post-plasma cell therapy in AL amyloid plaques and potential implications for light chaindirected anti-fibril monoclonal antibodies.Haematologica · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
backgroundCardiac AL and ATTR are potentially fatal cardiomyopathies. Current therapies do not address mechanisms of tissue dysfunction because these remain unknown. Our prior work focused on the amyloid plaque proteome, which may not capture tissue-wide proteomic alterations.
objectivesTo evaluate mechanisms of tissue dysfunction in cardiac AL and ATTR using a full biopsy tissue proteomics approach.
methodsWe performed proteomics analysis on 76 ATTR and 27 AL diagnostic endomyocardial biopsies.
resultsStage-3 AL patients exhibited increased coagulation, extracellular matrix remodelling (ECM), epithelial-to-mesenchymal transition (EMT), complement activation, hypoxia, and clathrin-mediated endocytosis pathways
conclusionsThis study identifies known processes dysregulated in heart failure with preserved ejection fraction as well as novel pathways responsible for tissue damage. Our results support an immune-mediated mechanism of tissue toxicity in cardiac amyloidosis, especially among patients with worse outcomes.
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Registered trials
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