ArticleBasic research in cardiology2013
Fibronectin contributes to pathological cardiac hypertrophy but not physiological growth.
Article in Basic research in cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- Exercise-induced cardiac hypertrophy: cellular and molecular mechanisms of cardiac adaptation following physical activity.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2026Review
- From bump to pump: extracellular matrix remodeling, dynamics, and biomechanics in the maternal heart.American journal of physiology. Heart and circulatory physiology · 2026Review
- Understanding Pathophysiological Complexity of Feline Hypertrophic Cardiomyopathy Using SWATH-MS Plasma Proteomics.Animals : an open access journal from MDPI · 2026Article
- Exploring Integrin α5β1 as a Potential Therapeutic Target for Pulmonary Arterial Hypertension: Insights From Comprehensive Multicenter Preclinical Studies.Circulation · 2025Article
- Matrisome remodeling in the myocardium of hypertrophic cardiomyopathy; novel targets for molecular diagnostics.Frontiers in cell and developmental biology · 2025Review
- Macrophages enhance sodium channel expression in cardiomyocytes.Basic research in cardiology · 2024Article
- SENP1-Mediated HSP90ab1 DeSUMOylation in Cardiomyocytes Prevents Myocardial Fibrosis by Paracrine Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The extent of postpartum cardiac reverse remodeling is reflected in urine proteome.Scientific reports · 2024Article
- Novel Multiplexed Plasma Biomarker Panel Has Diagnostic and Prognostic Potential in Children With Hypertrophic Cardiomyopathy.Circulation. Genomic and precision medicine · 2024Article
- Extracellular matrix-derived materials for tissue engineering and regenerative medicine: A journey from isolation to characterization and application.Bioactive materials · 2024Review
- Fibroblasts under pressure: cardiac fibroblast responses to hypertension and antihypertensive therapies.American journal of physiology. Heart and circulatory physiology · 2024Review
- Extracellular matrix remodelling in obesity and metabolic disorders.Life metabolism · 2023Article
- A Kinase Interacting Protein 1 (AKIP1) promotes cardiomyocyte elongation and physiological cardiac remodelling.Scientific reports · 2023Article
- Notch1 Is Involved in Physiologic Cardiac Hypertrophy of Mice via the p38 Signaling Pathway after Voluntary Running.International journal of molecular sciences · 2023Article
- The potential of remdesivir to affect function, metabolism and proliferation of cardiac and kidney cells in vitro.Archives of toxicology · 2022Article
- Animal Models of Exercise From Rodents to Pythons.Circulation research · 2022Review
- RBFOX2 is required for establishing RNA regulatory networks essential for heart development.Nucleic acids research · 2022Article
- Exploring the cardiac ECM during fibrosis: A new era with next-gen proteomics.Frontiers in molecular biosciences · 2022Review
- C-MORE: A high-content single-cell morphology recognition methodology for liquid biopsies toward personalized cardiovascular medicine.Cell reports. Medicine · 2021Article
- Discoidin Domain Receptor 2 Regulates AT1R Expression in Angiotensin II-Stimulated Cardiac Fibroblasts via Fibronectin-Dependent Integrin-β1 Signaling.International journal of molecular sciences · 2021Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Ability of the heart to undergo pathological or physiological hypertrophy upon increased wall stress is critical for long-term compensatory function in response to increased workload demand. While substantial information has been published on the nature of the fundamental molecular signaling involved in hypertrophy, the role of extracellular matrix protein Fibronectin (Fn) in hypertrophic signaling is unclear. The objective of the study was to delineate the role of Fn during pressure overload-induced pathological cardiac hypertrophy and physiological growth prompted by exercise. Genetic conditional ablation of Fn in adulthood blunts cardiomyocyte hypertrophy upon pressure overload via attenuated activation of nuclear factor of activated T cells (NFAT). Loss of Fn delays development of heart failure and improves survival. In contrast, genetic deletion of Fn has no impact on physiological cardiac growth induced by voluntary wheel running. Down-regulation of the transcription factor c/EBPβ (Ccaat-enhanced binding protein β), which is essential for induction of the physiological growth program, is unaffected by Fn deletion. Nuclear NFAT translocation is triggered by Fn in conjunction with up-regulation of the fetal gene program and hypertrophy of cardiomyocytes in vitro. Furthermore, activation of the physiological gene program induced by insulin stimulation in vitro is attenuated by Fn, whereas insulin had no impact on Fn-induced pathological growth program. Fn contributes to pathological cardiomyocyte hypertrophy in vitro and in vivo via NFAT activation. Fn is dispensable for physiological growth in vivo, and Fn attenuates the activation of the physiological growth program in vitro.
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Registered trials
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