ArticleAmerican journal of physiology. Heart and circulatory physiology2021
Transthyretin amyloid fibrils alter primary fibroblast structure, function, and inflammatory gene expression.
Article in American journal of physiology. Heart and circulatory physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Application of Omics Analysis in the Clinical Practice and Research of Transthyretin Amyloidosis.Genes · 2026Review
- Connexin 40 in atrial fibrillation: pathophysiological roles and regulatory mechanisms.Annals of medicine · 2025Review
- Profibrotic Biomarkers Correlate with Clinical Presentation and Outcome in Cardiac Transthyretin Amyloidosis.International journal of molecular sciences · 2025Article
- In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls, and potential.Cardiovascular research · 2025Review
- Uncovering cell type-specific phenotypes using a novel human in vitro model of transthyretin amyloid cardiomyopathy.Stem cell research & therapy · 2025Article
- Review
- Exploring Cardiac Sympathetic Denervation in Transthyretin-Mediated Hereditary Amyloidosis (ATTRv): Insights fromDiagnostics (Basel, Switzerland) · 2025Article
- Oxidative Stress in Transthyretin-Mediated Amyloidosis: An Exploratory Study.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Molecular mechanisms and emerging therapies in wild-type transthyretin amyloid cardiomyopathy.Heart failure reviews · 2024Review
- Sex differences in transthyretin cardiac amyloidosis.Heart failure reviews · 2024Review
- Inflammation across the spectrum of hypertrophic cardiac phenotypes.Heart failure reviews · 2023Review
- Microcalcification andInternational journal of molecular sciences · 2023Article
- Hereditary Transthyretin-Related Amyloidosis: Genetic Heterogeneity and Early Personalized Gene Therapy.Biomedicines · 2022Review
- Transthyretin deposition alters cardiomyocyte sarcomeric architecture, calcium transients, and contractile force.Physiological reports · 2022Article
- Proteomic analysis of serum samples of paracoccidioidomycosis patients with severe pulmonary sequel.PLoS neglected tropical diseases · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Age-related wild-type transthyretin amyloidosis (wtATTR) is characterized by systemic deposition of amyloidogenic fibrils of misfolded transthyretin (TTR) in the connective tissue of many organs. In the heart, this leads to cardiac dysfunction, which is a significant cause of age-related heart failure. The hypothesis tested is that TTR affects cardiac fibroblasts in ways that may contribute to fibrosis. When primary cardiac fibroblasts were cultured on TTR-deposited substrates, the F-actin cytoskeleton was disorganized, focal adhesion formation was decreased, and nuclear shape was flattened. Fibroblasts had faster collective and single-cell migration velocities on TTR-deposited substrates. In addition, fibroblasts cultured on microposts with TTR deposition had reduced attachment and increased proliferation above untreated. Transcriptomic and proteomic analyses of fibroblasts grown on glass covered with TTR showed significant upregulation of inflammatory genes after 48 h, indicative of progression in TTR-based diseases. Together, results suggest that TTR deposited in tissue extracellular matrix may affect the structure, function, and gene expression of cardiac fibroblasts. As therapies for wtATTR are cost-prohibitive and only slow disease progression, better understanding of cellular maladaptation may elucidate novel therapeutic targets.
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