ArticleJournal of the American College of Cardiology2017
Bone Marrow-Derived Tenascin-C Attenuates Cardiac Hypertrophy by Controlling Inflammation.
Article in Journal of the American College of Cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Single Cell and Spatial Transcriptomics Define a Proinflammatory and Profibrotic Niche After Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Anti-swelling and self-activating artificial proteoglycan assemblies as cartilaginous implant for post-microfracture healing.Nature communications · 2025Article
- Inhibition of tenascin C rescues abnormally reduced Na currents in dystrophin-deficient ventricular cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2025Article
- Protein Biomarkers of Adverse Clinical Features and Events in Sarcomeric Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2024Article
- The role of TNC in atherosclerosis and drug development opportunities.International journal of biological sciences · 2024Review
- Beyond the Rhythm: In Silico Identification of Key Genes and Therapeutic Targets in Atrial Fibrillation.Biomedicines · 2023Article
- Tenascin-C in fibrosis in multiple organs: Translational implications.Seminars in cell & developmental biology · 2022Review
- IntermedinInflammation · 2022Article
- Fibroblast mechanotransduction network predicts targets for mechano-adaptive infarct therapies.eLife · 2022Article
- Tenascin-C Participates Pulmonary Injury Induced by Paraquat Through Regulating TLR4 and TGF-β Signaling Pathways.Inflammation · 2022Article
- The Role of Matrix Proteins in Cardiac Pathology.International journal of molecular sciences · 2022Review
- Connecting different heart diseases through intercellular communication.Biology open · 2021Review
- Tenascin-C in Heart Diseases-The Role of Inflammation.International journal of molecular sciences · 2021Review
- Recombinant high‑mobility group box 1 induces cardiomyocyte hypertrophy by regulating the 14‑3‑3η, PI3K and nuclear factor of activated T cells signaling pathways.Molecular medicine reports · 2021Article
- The GABAFrontiers in immunology · 2021Article
- Effects of Tenascin C on the Integrity of Extracellular Matrix and Skin Aging.International journal of molecular sciences · 2020Article
- Adaptation within embryonic and neonatal heart environment reveals alternative fates for adult c-kitStem cells translational medicine · 2020Article
- Protective mechanism of SIRT1 on Hcy-induced atrial fibrosis mediated by TRPC3.Journal of cellular and molecular medicine · 2020Article
- The Roles of Tenascins in Cardiovascular, Inflammatory, and Heritable Connective Tissue Diseases.Frontiers in immunology · 2020Review
- Morphological and Functional Characteristics of Animal Models of Myocardial Fibrosis Induced by Pressure Overload.International journal of hypertension · 2020Review
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10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTenascin-C (TNC) is a highly conserved matricellular protein with a distinct expression pattern during development and disease. Remodeling of the left ventricle (LV) in response to pressure overload leads to the re-expression of the fetal gene program.
objectivesThe aim of this study was to investigate the function of TNC in cardiac hypertrophy in response to pressure overload.
methodsPressure overload was induced in TNC knockout and wild-type mice by constricting their abdominal aorta or by infusion of angiotensin II. Echocardiography, immunostaining, flow cytometry, quantitative real-time polymerase chain reaction, and reciprocal bone marrow transplantation were used to evaluate the effect of TNC deficiency.
resultsEchocardiographic analysis of pressure overloaded hearts revealed that all LV parameters (LV end-diastolic and -systolic dimensions, ejection fraction, and fractional shortening) deteriorated in TNC-deficient mice compared with their wild-type counterparts. Cardiomyocyte size and collagen accumulation were significantly greater in the absence of TNC. Mechanistically, TNC deficiency promoted rapid accumulation of the CCR2
conclusionsTNC deficiency further impaired cardiac function in response to pressure overload and exacerbated fibrosis by enhancing inflammation. In addition, expression of TNC in the bone marrow, but not the myocardium, protected the myocardium against excessive remodeling in response to mild pressure overload.
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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.