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Animal models have provided invaluable tools in improving our understanding of cardiac physiology and the mechanisms underlying heart disease. Until recently, available models were generated by surgical or pharmacological interventions or were the result of random genetic events, which made it difficult to establish a direct relationship between structural changes and functional alterations (1). However, the advancements in our ability to genetically manipulate the mammalian genome through transgenesis and gene targeting have provided important insights into thein vivo structure-function relation and interaction of specific gene products. Furthermore, genetically altered animals offer unique opportunities to identify genes that are causative for certain diseases, to evaluate molecular mechanisms responsible for the development and progression of diseases, and finally, to test new therapeutic strategies (2). In this regard, the mouse has emerged as the premier mammalian model system since it allows precise manipulation of its genome, has a short gestation period and its genetics and development have been well characterized (3). Initially, the small size of the murine heart was a challenging and limiting factor in the physiological and pathophysiological evaluation of phenotypic cardiac alterations. However, advances in “microphysiology” provided us with various techniques to assess cardiac function in an integrative approach from the cellular to the intact animal levels (4). |
