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See article by Bluhm et al. [18] (pages 382–388) in this issue. Recent advances in animal genetics and transgenic technology have blossomed into one of the dominant strategies to explore the consequences of gene defects in different organ systems in the in vivo context. Such a perspective has been progressively applied to the cardiovascular system to dissect complex in vivo physiologic and pathologic states. The encouraging results achieved so far in the field of heart hypertrophy and failure with the aid of engineered mouse models have even suggested consideration for the cardiovascular system as a paradigm for other complex apparata, including the pulmonary, renal and neural systems [1].It is now becoming increasingly evident that the myocardial cell, besides being a target for a number of hormones and growth factors [2,3] also behaves as a source for peptides that may play a crucial role in signal transduction processes in the heart [4–7]. Hence, the myocardium adapts to hormonal, genetic and mechanical stimuli by triggering a number of paracrine, autocrine and intracrine responses that represent the plight that is impacting the homeostasis of the myocardial cells throughout specific pathologic processes [8–11]. The complexity of the overall picture is given by the finding that heart mechanical dysfunctions and failure are often the functional end-point of processes involving an impairment of the architectural plan of the myocardial cell [1,12]. … * Corresponding author

Sarcoplasmic reticulum Ca2+ ATPase gene expression to the rescue of myocardial contractility in hypothyroid associated heart failure