ArticleJACC. CardioOncology2020
A Proteomic Atlas of Cardiac Amyloid Plaques.
Article in JACC. CardioOncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 50 citations in OpenAlex.
- Proteomics Profiling Reveals Molecular Subtypes of Transthyretin Cardiac Amyloidosis.Circulation. Heart failure · 2026Article
- Reversing the pipeline: a 'human-first' multi-omics approach to cardiovascular discovery.Experimental & molecular medicine · 2026Review
- Transthyretin Cardiac Amyloidosis in Women: Underdiagnosis, Sex-Specific Phenotypic Expression and Therapeutic Response.Journal of clinical medicine · 2026Review
- 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
- Application of Omics Analysis in the Clinical Practice and Research of Transthyretin Amyloidosis.Genes · 2026Review
- Current Standards and Perspectives in Proteomics for Cardiac Amyloidosis.Analytical chemistry · 2026Review
- Basal inferoseptal longitudinal strain deformation may indicate early cardiac involvement in wild-type carpal ATTR.ESC heart failure · 2026Article
- 3D Visualization and Proteomic Analysis of Human Cardiac Transthyretin Amyloidosis Tissue Reveals Microangiopathy and Capillary Occlusion.bioRxiv : the preprint server for biology · 2026Article
- Proteomic shifts post-plasma cell therapy in AL amyloid plaques and potential implications for light chaindirected anti-fibril monoclonal antibodies.Haematologica · 2026Article
- Single-cell and clonal analysis of AL amyloidosis plasma cells and their bone marrow microenvironment.Blood · 2025Article
- Article
- The molecular landscape of AL amyloidosis.British journal of haematology · 2025Review
- Integrating -Omic Technologies across Modality, Space, and Time to Decipher Remodeling in Cardiac Disease.Current cardiology reports · 2025Review
- 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
- Computational Tools and Methods for the Study of Systemic Amyloidosis at the Clinical and Molecular Level.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Circulating ECM proteins decorin and alpha-L-iduronidase differentiate ATTRwt-CM from ATTRwt-negative HFpEF/HFmrEF.Cardiovascular research · 2024Observational
- Myocardial inflammatory cells in cardiac amyloidosis.Scientific reports · 2024Article
- Integrative proteomics identifies a conserved Aβ amyloid responsome, novel plaque proteins, and pathology modifiers in Alzheimer's disease.Cell reports. Medicine · 2024Article
- Effect of dynamic exclusion and the use of FAIMS, DIA and MALDI-mass spectrometry imaging with ion mobility on amyloid protein identification.Clinical proteomics · 2024Article
Corrections and comments
- Commented on by
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIn vivo mechanisms of amyloid clearance and cardiac tissue damage in cardiac amyloidosis are not well understood.
objectivesWe aimed to define and quantify the amyloid plaque proteome in cardiac transthyretin amyloidosis (ATTR) and light chain amyloidosis (AL) and identify associations with patient characteristics and outcomes.
methodsA proteomics approach was used to identify all proteins in cardiac amyloid plaques, and to compare both normal and diseased controls. All proteins identified within amyloid plaques were defined as the expanded proteome; only proteins that were enriched in comparison to normal and disease controls were defined as the amyloid-specific proteome.
resultsProteomic data from 292 patients with ATTR and 139 patients with AL cardiac amyloidosis were included; 160 and 161 unique proteins were identified in the expanded proteomes, respectively. In the amyloid-specific proteomes, we identified 28 proteins in ATTR, 19 in AL amyloidosis, with 13 proteins overlapping between ATTR and AL. ATTR was characterized by a higher abundance of complement and contractile proteins and AL by a higher abundance of keratins. We found that the proteome of kappa AL had higher levels of clusterin, a protective chaperone, and lower levels of light chains than lambda despite higher levels of circulating light chains. Hierarchical clustering identified a group of patients with worse survival in ATTR, characterized by high levels of PIK3C3, a protein with a central role in autophagy.
conclusionsCardiac AL and ATTR have both common and distinct pathogenetic mechanisms of tissue damage. Our findings suggest that autophagy represents a pathway that may be impaired in ATTR and should be further studied.
Indexed as
Identifiers
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.