ArticleCirculation2012
Reduced endoglin activity limits cardiac fibrosis and improves survival in heart failure.
Article in Circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
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Who cites it
61 citing papers in PubMed, 122 citations in OpenAlex.
- Sex-dependent epigenomic and transcriptomic reprogramming links maternal obesity to cardiac remodeling in adult offspring.American journal of physiology. Heart and circulatory physiology · 2026Article
- Genome-wide analysis of cardiac ventricular phenotypes reveals novel loci and therapeutic targets for heart failure.Nature communications · 2026Article
- Pretreatment Circulating Vascular Biomarkers Predict Cancer Therapy-Related Cardiac Dysfunction During HER2JACC. CardioOncology · 2025Article
- Coordinated expression of BMP10/ALK1/endoglin-proteins that drive embryonic cardiac and vascular morphogenesis-in patients with heart failure: The EMPEROR Program.European journal of heart failure · 2025Article
- High-Fat Diet Augments Myocardial Inflammation and Cardiac Dysfunction in Arrhythmogenic Cardiomyopathy.Nutrients · 2024Article
- Machine learning in heart failure diagnosis, prediction, and prognosis: review.Annals of medicine and surgery (2012) · 2024Review
- Circulating GDF11 exacerbates myocardial injury in mice and associates with increased infarct size in humans.Cardiovascular research · 2023Article
- High concentrations of soluble endoglin can inhibit BMP9 signaling in non-endothelial cells.Scientific reports · 2023Article
- Endoglin Is an Important Mediator in the Final Common Pathway of Chronic Kidney Disease to End-Stage Renal Disease.International journal of molecular sciences · 2022Article
- Smad3 promotes adverse cardiovascular remodeling and dysfunction in doxorubicin-treated hearts.American journal of physiology. Heart and circulatory physiology · 2022Article
- Progressive stages of dysmetabolism are associated with impaired biological features of human cardiac stromal cells mediated by the oxidative state and autophagy.The Journal of pathology · 2022Article
- Targeting Myocardial Fibrosis-A Magic Pill in Cardiovascular Medicine?Pharmaceutics · 2022Review
- Transforming growth factor-β in myocardial disease.Nature reviews. Cardiology · 2022Review
- Myocardial Injury Promotes Matrix Metalloproteinase-9 Activity in the Renal Cortex in Preclinical Models of Acute Myocardial Infarction.Journal of cardiovascular translational research · 2022Article
- Endoglin aggravates peritoneal fibrosis by regulating the activation of TGF-β/ALK/Smads signaling.Frontiers in pharmacology · 2022Article
- Endothelial Activin Receptor-Like Kinase 1 (ALK1) Regulates Myofibroblast Emergence and Peritubular Capillary Stability in the Early Stages of Kidney Fibrosis.Frontiers in pharmacology · 2022Article
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Membrane and soluble endoglin role in cardiovascular and metabolic disorders related to metabolic syndrome.Cellular and molecular life sciences : CMLS · 2021Review
- The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure.Cell & bioscience · 2021Article
- Cardiac Fibrosis: Cellular Effectors, Molecular Pathways, and Exosomal Roles.Frontiers in cardiovascular medicine · 2021Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundHeart failure is a major cause of morbidity and mortality worldwide. The ubiquitously expressed cytokine transforming growth factor-β1 (TGFβ1) promotes cardiac fibrosis, an important component of progressive heart failure. Membrane-associated endoglin is a coreceptor for TGFβ1 signaling and has been studied in vascular remodeling and preeclampsia. We hypothesized that reduced endoglin expression may limit cardiac fibrosis in heart failure. METHODS AND
resultsWe first report that endoglin expression is increased in the left ventricle of human subjects with heart failure and determined that endoglin is required for TGFβ1 signaling in human cardiac fibroblasts using neutralizing antibodies and an siRNA approach. We further identified that reduced endoglin expression attenuates cardiac fibrosis, preserves left ventricular function, and improves survival in a mouse model of pressure-overload-induced heart failure. Prior studies have shown that the extracellular domain of endoglin can be cleaved and released into the circulation as soluble endoglin, which disrupts TGFβ1 signaling in endothelium. We now demonstrate that soluble endoglin limits TGFβ1 signaling and type I collagen synthesis in cardiac fibroblasts and further show that soluble endoglin treatment attenuates cardiac fibrosis in an in vivo model of heart failure.
conclusionOur results identify endoglin as a critical component of TGFβ1 signaling in the cardiac fibroblast and show that targeting endoglin attenuates cardiac fibrosis, thereby providing a potentially novel therapeutic approach for individuals with heart failure.
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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.