Abstract
Spinal muscular atrophy (SMA) is an autosomal recessive inherited neuromuscular disease and is the most frequent genetic cause of death in infancy. SMA is caused by a ubiquitous lack of SMN protein which leads primarily to an irreversible loss of motor neurons, but development or function of other tissues may also be affected. In mouse models the most prominent microscopic findings were myocardial fibrosis, decreased numbers of coronary capillaries, and abnormal expression of postnatal cardiac development markers indicating loss of contractile components.
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