Key result
Ras activation in a transgenic mouse model induced hypertrophic cardiomyopathy with depressed calcium transients, reduced SERCA2a expression, and hypophosphorylation of PLB.
Why the study?
Does Ras activation alter cellular calcium handling and sarcomere organization in adult ventricular myocytes?
Does Ras activation alter cellular calcium handling and sarcomere organization in adult ventricular myocytes?
Ras-induced hypertrophic cardiomyopathy and diastolic dysfunction are associated with suppressed SR calcium uptake due to reduced SERCA2a expression and hypophosphorylation of PLB, rather than decreased L-type calcium channel activities or sarcomere disruption.
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Ras-mediated calcium defects in murine HCM; hypothesis-generating for human mechanisms and requires validation before clinical relevance.
Zheng et al. (2004) studied Hypertrophic cardiomyopathy and heart failure. Targeted expression of the H-Ras-v12 mutant (Ras activation) vs. Control littermates was evaluated on Cellular calcium handling and sarcomere organization. Ras activation in a transgenic mouse model induced hypertrophic cardiomyopathy with depressed calcium transients, reduced SERCA2a expression, and hypophosphorylation of PLB.
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