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Tenascin-C is an extracellular matrix glycoprotein that is specifically and transiently expressed upon tissue injury. Upon tissue damage, tenascin-C plays a multitude of different roles that mediate both inflammatory and fibrotic processes to enable effective tissue repair. In the last decade, emerging evidence has demonstrated a vital role for tenascin-C in cardiac and arterial injury, tumor angiogenesis and metastasis, as well as in modulating stem cell behavior. Here we highlight the molecular mechanisms by which tenascin-C mediates these effects and discuss the implications of mis-regulated tenascin-C expression in driving disease pathology.

Type

Journal article

Journal

Cellular and molecular life sciences : CMLS

Publication Date

10/2011

Volume

68

Pages

3175 - 3199

Addresses

Kennedy Institute of Rheumatology Division, Faculty of Medicine, NDORMS, Oxford University, 65 Aspenlea Road, Hammersmith, London W6 8LH, UK. kim.midwood@kennedy.ox.ac.uk

Keywords

Myocardium, Myocytes, Smooth Muscle, Stem Cells, Animals, Humans, Mice, Rats, Neoplasms, Myocardial Infarction, Vascular Diseases, Neovascularization, Pathologic, Tenascin, Wound Healing, Gene Expression Regulation, Atherosclerosis, Neoplastic Stem Cells