ArticleBiomaterials2020
Lack of Thy1 defines a pathogenic fraction of cardiac fibroblasts in heart failure.
Article in Biomaterials, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 46 citations in OpenAlex.
- An ALMS1 variant disrupts proximal centriole organization and promotes a myofibroblast-like phenotype that is regulated by THY1.Research square · 2026Article
- Targeting fibroblasts in immune mediated inflammatory diseases: a cellular basis for cure?Rheumatology (Oxford, England) · 2026Review
- Bioinformatics and Immunohistochemistry Reveal the Diagnostic and Mechanistic Role of the Cuproptosis-Related Genes SMOC2/THY1 in Liver Fibrosis.Journal of cellular and molecular medicine · 2026Article
- Regulation of sodium/calcium homeostasis by BacNaScience advances · 2026Article
- Interleukin-6 blockade modulates monocyte recruitment to protect against diastolic dysfunction associated with inflammatory arthritis.Arthritis research & therapy · 2026Article
- Targeting Cardiac Fibroblast Plasticity for Antifibrotic and Regenerative Therapy in Heart Failure.Cells · 2026Review
- Article
- Uncovering key markers and therapeutic targets for renal fibrosis in diabetic kidney disease through bulk and single-cell RNA sequencing.Journal of translational medicine · 2025Article
- Targeting cardiac fibrosis with Chimeric Antigen Receptor-Engineered Cells.Molecular and cellular biochemistry · 2025Review
- Exploring the Role of Thy-1 and Its Soluble Form Regarding Fibrosis Severity in Primary Biliary Cholangitis and Metabolic Dysfunction-Associated Fatty Liver Disease.JGH open : an open access journal of gastroenterology and hepatology · 2025Article
- A Thy-1-negative immunofibroblast population emerges as a key determinant of fibrotic outcomes to biomaterials.Science advances · 2024Article
- Identification of diagnostic model in heart failure with myocardial fibrosis and conduction block by integrated gene co-expression network analysis.BMC medical genomics · 2024Article
- Time-dependent effects of BRAF-V600E on cell cycling, metabolism, and function in engineered myocardium.Science advances · 2024Article
- A division-of-labor mode contributes to the cardioprotective potential of mesenchymal stem/stromal cells in heart failure post myocardial infarction.Frontiers in immunology · 2024Article
- Microarray-based Detection of Critical Overexpressed Genes in the Progression of Hepatic Fibrosis in Non-alcoholic Fatty Liver Disease: A Protein-protein Interaction Network Analysis.Current medicinal chemistry · 2024Article
- Antifibrotic Soluble Thy-1 Correlates with Renal Dysfunction in Chronic Kidney Disease.International journal of molecular sciences · 2023Article
- Cardiac Disease Modeling with Engineered Heart Tissue.Handbook of experimental pharmacology · 2023Review
- Neuregulin (NRG-1β) Is Pro-Myogenic and Anti-Cachectic in Respiratory Muscles of Post-Myocardial Infarcted Swine.Biology · 2022Article
- Hif-1a suppresses ROS-induced proliferation of cardiac fibroblasts following myocardial infarction.Cell stem cell · 2022Article
- A three-dimensional culture system for generating cardiac spheroids composed of cardiomyocytes, endothelial cells, smooth-muscle cells, and cardiac fibroblasts derived from human induced-pluripotent stem cells.Frontiers in bioengineering and biotechnology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In response to heart injury, inflammation, or mechanical overload, quiescent cardiac fibroblasts (CFs) can become activated myofibroblasts leading to pathological matrix remodeling and decline in cardiac function. Specific targeting of fibroblasts may thus enable new therapeutic strategies to delay or reverse the progression of heart failure and cardiac fibrosis. However, it remains unknown if all CFs are equally responsive to specific pathological insults and if there exist sub-populations of resident fibroblasts in the heart that have distinctive pathogenic phenotypes. Here, we show that in response to transverse aortic constriction (TAC)-induced heart failure, previously uncharacterized Thy1
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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.