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Wnt-1 dishevelled signaling functionally links calcium-calmodulin-dependent protein kinase II and cardiac dysfunction.

See related article, pp 335–344

Shortly after birth the cardiac muscle cells exit the cell cycle and lose their ability to replicate. Hence, growth of the postnatal heart occurs by hypertrophic rather than hyperplasic processes.1 This basic biological fact has profound clinical implications because the functional loss of cardiac myocytes by apoptosis or necrosis after injury triggers the adjacent myocardium to hypertrophy as means to off-set the increased wall stress. However, in some individuals, for reasons unknown, this adaptive process of compensatory cardiac hypertrophy fails ultimately resulting in overt heart failure. For this reason, there has been tremendous interest during the past 2 decades of heart research focused at deciphering the signaling pathways and molecular effectors that underlie cardiac hypertrophy and heart failure.

In this regard, early studies in fruit flies and worms led to the discovery of the Wnt signaling pathway as a central regulator of embryonic development and cell growth.2 Importantly, the Wnt receptor Frizzled and cytoplasmic scaffold protein Dishevelled (Dvl) together with β-catenin have been linked to embryo cardiogenesis as well as cellular processes involved in physiological hypertrophy of the postnatal adult heart.3 However, a growing body of experimental evidence suggests involvement of both canonical and noncanonical Wnt signaling pathways in the development of pathological cardiac hypertrophy.3 Classically, activation of the canonical Wnt signaling involves …