ArticleInternational journal of molecular sciences2021
The Role of Tenascin C in Cardiac Reverse Remodeling Following Banding-Debanding of the Ascending Aorta.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Tenascin C promotes the formation of abdominal aortic aneurysm by regulating the homeostasis of vascular smooth muscle cells.Biology direct · 2026Article
- Vascular (dys)function in the failing heart.Nature reviews. Cardiology · 2025Review
- 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
- Beyond the Rhythm: In Silico Identification of Key Genes and Therapeutic Targets in Atrial Fibrillation.Biomedicines · 2023Article
- Overlapping and Distinct Features of Cardiac Pathology in Inherited Human and Murine Ether Lipid Deficiency.International journal of molecular sciences · 2023Article
- Alterations in Coronary Resistance Artery Network Geometry in Diabetes and the Role of Tenascin C.Reviews in cardiovascular medicine · 2023Article
- Concomitant elevated serum levels of tenascin, MMP-9 and YKL-40, suggest ongoing remodeling of the heart up to 3 months after cardiac surgery after normalization of the revascularization markers.European journal of medical research · 2022Article
- Hypertension and Cardiovascular Diseases: From Etiopathogenesis to Potential Therapeutic Targets.International journal of molecular sciences · 2022Article
- The expression and role of tenascin C in abdominal aortic aneurysm formation and progression.Interactive cardiovascular and thoracic surgery · 2022Article
- Single Donor Infusion of S-Nitroso-Human-Serum-Albumin Attenuates Cardiac Isograft Fibrosis and Preserves Myocardial Micro-RNA-126-3p in a Murine Heterotopic Heart Transplant Model.Transplant international : official journal of the European Society for Organ Transplantation · 2022Article
- Tenascin-C in Heart Diseases-The Role of Inflammation.International journal of molecular sciences · 2021Review
- Cellular and Molecular Mechanism of Traditional Chinese Medicine on Ventricular Remodeling.Frontiers in cardiovascular medicine · 2021Review
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundTenascin-C (TN-C) plays a maladaptive role in left ventricular (LV) hypertrophy following pressure overload. However, the role of TN-C in LV regression following mechanical unloading is unknown.
methodsLV hypertrophy was induced by transverse aortic constriction for 10 weeks followed by debanding for 2 weeks in wild type (Wt) and TN-C knockout (TN-C KO) mice. Cardiac function was assessed by serial magnetic resonance imaging. The expression of fibrotic markers and drivers (angiotensin-converting enzyme-1, ACE-1) was determined in LV tissue as well as human cardiac fibroblasts (HCFs) after TN-C treatment.
resultsChronic pressure overload resulted in a significant decline in cardiac function associated with LV dilation as well as upregulation of TN-C, collagen 1 (Col 1), and ACE-1 in Wt as compared to TN-C KO mice. Reverse remodeling in Wt mice partially improved cardiac function and fibrotic marker expression; however, TN-C protein expression remained unchanged. In HCF, TN-C strongly induced the upregulation of ACE 1 and Col 1.
conclusionsPressure overload, when lasting long enough to induce HF, has less potential for reverse remodeling in mice. This may be due to significant upregulation of TN-C expression, which stimulates ACE 1, Col 1, and alpha-smooth muscle actin (α-SMA) upregulation in fibroblasts. Consequently, addressing TN-C in LV hypertrophy might open a new window for future therapeutics.
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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.