ArticleESC heart failure2020
Tenascin-C aggravates ventricular dilatation and angiotensin-converting enzyme activity after myocardial infarction in mice.
Article in ESC heart failure, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Inhibition of tenascin C rescues abnormally reduced Na currents in dystrophin-deficient ventricular cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2025Article
- Tenascin-C drives cardiovascular dysfunction in a mouse model of diabetic cardiomyopathy.Cardiovascular diabetology · 2025Article
- Molecular Imaging of Fibroblast Activation Protein in Response to Cardiac Injury Using [Pharmaceuticals (Basel, Switzerland) · 2025Article
- The diagnostic value of tenascin-C in acute aortic syndrome.Journal of geriatric cardiology : JGC · 2024Article
- Association ofGenetic testing and molecular biomarkers · 2024Article
- Regulation of toll-like receptor (TLR) signaling pathways in atherosclerosis: from mechanisms to targeted therapeutics.Acta pharmacologica Sinica · 2023Review
- Alterations in Coronary Resistance Artery Network Geometry in Diabetes and the Role of Tenascin C.Reviews in cardiovascular medicine · 2023Article
- Diagnostic value of myocardial stress detection based on feature tracking MRI in patients with acute myocardial infarction.Journal of thoracic disease · 2022Article
- The expression and role of tenascin C in abdominal aortic aneurysm formation and progression.Interactive cardiovascular and thoracic surgery · 2022Article
- Alterations in ACE and ACE2 Activities and Cardiomyocyte Signaling Underlie Improved Myocardial Function in a Rat Model of Repeated Remote Ischemic Conditioning.International journal of molecular sciences · 2021Article
- Connecting different heart diseases through intercellular communication.Biology open · 2021Review
- Involvement of the extracellular matrix proteins periostin and tenascin C in nasal polyp remodeling by regulating the expression of MMPs.Clinical and translational allergy · 2021Article
- Tenascin-C in Heart Diseases-The Role of Inflammation.International journal of molecular sciences · 2021Review
- Identification of key genes in calcific aortic valve disease via weighted gene co-expression network analysis.BMC medical genomics · 2021Article
- Cardiovascular phenotype of theDisease models & mechanisms · 2021Article
- The Role of Tenascin C in Cardiac Reverse Remodeling Following Banding-Debanding of the Ascending Aorta.International journal of molecular sciences · 2021Article
- Tenascin-C aggravates ventricular dilatation and angiotensin-converting enzyme activity after myocardial infarction in mice.ESC heart failure · 2020Article
- The Roles of Tenascins in Cardiovascular, Inflammatory, and Heritable Connective Tissue Diseases.Frontiers in immunology · 2020Review
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
aimsTenascin-C (TN-C) is suggested to be detrimental in cardiac remodelling after myocardial infarction (MI). The aim of this study is to reveal the effects of TN-C on extracellular matrix organization and its haemodynamic influence in an experimental mouse model of MI and in myocardial cell culture during hypoxic conditions. METHODS AND
resultsMyocardial infarction was induced in TN-C knockout (TN-C KO) and wild-type mice. Six weeks later, cardiac function was studied by magnetic resonance imaging and under isolated working heart conditions. Myocardial mRNA levels and immunoreactivity of TN-C, TIMP-1, TIMP-3, and matrix metalloproteinase (MMP)-9, as well as serum and tissue activities of angiotensin-converting enzyme (ACE), were determined at 1 and 6 weeks after infarction. Cardiac output and external heart work were higher, while left ventricular wall stress and collagen expression were decreased (P < 0.05) in TN-C KO mice as compared with age-matched controls at 6 weeks after infarction. TIMP-1 expression was down-regulated at 1 and 6 weeks, and TIMP-3 expression was up-regulated at 1 week (P < 0.01) after infarction in knockout mice. MMP-9 level was lower in TN-C KO at 6 weeks after infarction (P < 0.05). TIMP-3/MMP-9 ratio was higher in knockout mice at 1 and 6 weeks after infarction (P < 0.01). ACE activity in the myocardial border zone (i.e. between scar and free wall) was significantly lower in knockout than in wild-type mice 1 week after MI (P < 0.05).
conclusionsTenascin-C expression is induced by hypoxia in association with ACE activity and MMP-2 and MMP-9 elevations, thereby promoting left ventricular dilatation after MI.
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