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. Author manuscript; available in PMC: 2015 Apr 27.
Published in final edited form as: Physiol Rev. 2012 Apr;92(2):635–688. doi: 10.1152/physrev.00008.2011

Table 3.

Role of the tenascins in normal and diseased hearts

Tenascin-C Tenascin-X
Role in cardiac homeostasis In the normal adult myocardium tenascin-C expression is found only at the chordate tendinae of the papillary muscles (383). There is no known role for tenascin-C in cardiac homeostasis. Tenascin-X is abundantly expressed in the normal adult heart (287). However, tenascin-X absence did not result in any gross cardiac abnormalities (279). Systematic studies of cardiac function and geometry in tenascin-X null mice have not been reported.
Role in cardiac aging No known role. Not known.
Role in myocardial infarction Tenascin-C is markedly upregulated in the infarcted myocardium and is predominantly localized in the border zone and in remodelling areas (190). Tenascin-C −/− mice are protected from adverse post-infarction remodeling and have reduced fibrosis in the non-infarcted areas (323). The detrimental effects of tenascin-C in the healing infarct may be mediated through accentuation of pro-fibrotic growth factor signalling. Not known.
Role in cardiac hypertrophy and fibrosis Tenascin-C is upregulated in the pressure-overloaded myocardium (491). However, its role in hypertrophy and fibrosis is unknown. Not known.
Role in myocarditis, cardiomyopathies and cardiac allograft Tenascin-C upregulation is a hallmark of cardiac remodelling regardless of etiology. Tenascin-C induction was reported in autoimmune myocarditis (191). In a model of cardiac transplantation, tenascin-C null mice had impaired allograft vascularisation (28). Not known.
Tenascins in human heart disease Tenascin-C upregulation is consistently found in human cardiomyopathic hearts and is a marker of active remodeling (149). Tenascin-C has potential as a marker of disease activity (reflecting inflammation, fibrosis and remodeling) in human myocarditis and cardiomyopathy (300), (382). Occasional cases of valvular disease have been reported in human patients with tenascin-X deficiency, a condition that causes a distinct form of the Ehlers-Danlos syndrome (347).