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64. Nagata S, Park Y, Minamikawa T, Yutani C, Kamiya T, Nishimura T, Kozuka T, Sakakibara H, Nimura Y. Thallium perfusion and cardiac enzyme abnormalities in patients with familial hypertrophic cardiomyopathy. Am Heart J 1985; 109(6):1317–1322. 65. Ashrafian H, Redwood C, Blair E, Watkins H. Hypertrophic cardiomyopathy: a paradigm for myocardial energy depletion. Trends Genet 2003; 19(5):263–268. 66. Geisterfer-Lowrance AA, Kass S, Tanigawa G, Vosberg HP, McKenna W, Seidman CE, Seidman JG. A molecular basis for familial hypertrophic cardiomyopathy: a beta cardiac myosin heavy chain gene missense mutation.

Transactivation of the EGF receptor was originally noted by Ullrich and co-workers in 1996 [15]. The current model involves calcium transient-induced (and possibly oxidant stress-induced [16]) activation of a metalloprotease that releases heparin-binding EGFlike growth factor, which then binds to the receptor, activating additional signaling pathways not directly activated by the Ang II receptor [17,18]. A second group of factors released by mechanical stretch are the IL-6 family of cytokines, including cardiotrophin1 (CT-1), which act via receptors specific to the cytokine and via the common receptor, gp130 [19–21].

Eur Heart J 1996; 17(7):1056–1064. 64. Nagata S, Park Y, Minamikawa T, Yutani C, Kamiya T, Nishimura T, Kozuka T, Sakakibara H, Nimura Y. Thallium perfusion and cardiac enzyme abnormalities in patients with familial hypertrophic cardiomyopathy. Am Heart J 1985; 109(6):1317–1322. 65. Ashrafian H, Redwood C, Blair E, Watkins H. Hypertrophic cardiomyopathy: a paradigm for myocardial energy depletion. Trends Genet 2003; 19(5):263–268. 66. Geisterfer-Lowrance AA, Kass S, Tanigawa G, Vosberg HP, McKenna W, Seidman CE, Seidman JG.

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