April 13, 2007Journal of Clinical InvestigationOpen Access

Early cardiac hypertrophy in mice with impaired calmodulin regulation of cardiac muscle Ca2+ release channel

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Population

Mice generated with 3 amino acid substitutions in exon 75 of the Ryr2 gene, which encodes the CaM-binding…

Design

Preclinical

Follow-up

Up to 16 days of age

Authors

NYNaohiro YamaguchiUniversity of Delhi NTNobuyuki TakahashiUniversity of North Carolina at Chapel Hill LXLe XuChina West Normal University

Discussion

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Implication

Loss of calmodulin-RyR2 inhibition causes lethal cardiomyopathy in mice; leaves open relevance to human disease and targeted therapies.

Structured PICO

Population

Mice generated with 3 amino acid substitutions (RyR2-W3587A/L3591D/F3603A) in exon 75 of the Ryr2 gene, which encodes the CaM-binding site of RyR2

Intervention

Homozygous mutation impairing calmodulin (CaM) regulation of the cardiac muscle cell Ca2+ release channel ryanodine receptor 2 (RyR2)

Outcome

Cardiac hypertrophy (ratio of heart weight to body weight), fractional shortening of the left ventricle, and lethalitysurrogate

Impaired calmodulin inhibition of the RyR2 calcium release channel leads to defective calcium handling, cardiac hypertrophy, and early death in a mouse model.

Cite This Study

Yamaguchi et al. (2007) studied this question.

synapsesocial.com/papers/6a76a8fb2ea07b97ffadf3ea https://doi.org/10.1172/jci29515

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Early cardiac hypertrophy in mice with impaired calmodulin regulation of cardiac muscle Ca2+ release channel

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Early cardiac hypertrophy in mice with impaired calmodulin regulation of cardiac muscle Ca2+ release channel

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider