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). |