Population
Transgenic rats overexpressing alpha-tropomyosin with disease-causing mutations Asp(175)Asn or Glu(180)Gly
Design
Preclinical
Authors
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Animal model data should not change HCM practice; leaves open mutation-specific Ca2+ mechanisms pending human validation.
The Asp(175)Asn mutation in alpha-tropomyosin alters Ca2+ handling to compensate for reduced Ca2+ sensitivity, providing mechanistic insight into the pathogenesis of familial hypertrophic cardiomyopathy.
Wernicke et al. (2004) studied this question.
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