ArticleNature cardiovascular research2025
ANTXR1 blockade enhances cardiac function in preclinical models of heart failure.
Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Right ventricular pressure overload disturbs T-tubule maturation via MEF2D's transcriptional regulation of BIN1.JCI insight · 2026Article
- Cardiac fibroblast diversity in HFpEF: states, niches, interorgan drivers and targets.Nature reviews. Cardiology · 2026Review
- Accelerated Turnover of Collagens and Other Extracellular Matrix Proteins Upon Chronic Beta-Adrenergic Stimulation.JACC. Basic to translational science · 2026Article
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart disease, a leading cause of mortality worldwide, is in urgent need of improved therapies. Fibrosis, an accumulation of collagen-rich extracellular matrix in response to injury, is a hallmark of heart disease, but clinical agents that can interfere with the fibrotic pathway do not yet exist. Here we show that ANTXR1/TEM8, a pathology-induced transmembrane protein required for collagen removal, exacerbates injury in multiple models of heart failure. Genetic disruption of Antxr1 and treatment with human neutralizing antibodies prevented heart deterioration following acute myocardial infarction. ANTXR1 pharmacological blockade also improved heart function in models of pressure overload and obesity-induced heart disease with preserved ejection fraction. Improved heart function was accompanied by enhanced exercise tolerance. Mechanistic studies revealed an ANTXR1-antibody-driven improvement in post-infarct scar formation followed by attenuation of late-stage, chronic TGFβ-mediated extracellular matrix remodeling. Thus, ANTXR1-mediated collagen turnover during heart failure is both maladaptive and druggable, providing avenues for therapeutic intervention.
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