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Tenascin-C in Heart Diseases-The Role of Inflammation.

Abstract
Tenascin-C (TNC) is a large extracellular matrix (ECM) glycoprotein and an original member of the matricellular protein family. TNC is transiently expressed in the heart during embryonic development, but is rarely detected in normal adults; however, its expression is strongly up-regulated with inflammation. Although neither TNC-knockout nor -overexpressing mice show a distinct phenotype, disease models using genetically engineered mice combined with in vitro experiments have revealed multiple significant roles for TNC in responses to injury and myocardial repair, particularly in the regulation of inflammation. In most cases, TNC appears to deteriorate adverse ventricular remodeling by aggravating inflammation/fibrosis. Furthermore, accumulating clinical evidence has shown that high TNC levels predict adverse ventricular remodeling and a poor prognosis in patients with various heart diseases. Since the importance of inflammation has attracted attention in the pathophysiology of heart diseases, this review will focus on the roles of TNC in various types of inflammatory reactions, such as myocardial infarction, hypertensive fibrosis, myocarditis caused by viral infection or autoimmunity, and dilated cardiomyopathy. The utility of TNC as a biomarker for the stratification of myocardial disease conditions and the selection of appropriate therapies will also be discussed from a clinical viewpoint.
AuthorsKyoko Imanaka-Yoshida
JournalInternational journal of molecular sciences (Int J Mol Sci) Vol. 22 Issue 11 (May 29 2021) ISSN: 1422-0067 [Electronic] Switzerland
PMID34072423 (Publication Type: Journal Article, Review)
Chemical References
  • Biomarkers
  • TNC protein, human
  • Tenascin
Topics
  • Animals
  • Biomarkers
  • Biopsy
  • Disease Management
  • Disease Susceptibility
  • Fibrosis
  • Gene Expression
  • Gene Expression Regulation
  • Heart Diseases (diagnosis, etiology, metabolism)
  • Humans
  • Myocarditis (diagnosis, etiology, metabolism)
  • Organogenesis (genetics)
  • Prognosis
  • Signal Transduction
  • Tenascin (genetics, metabolism)
  • Ventricular Remodeling (genetics)

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