January 1, 2018Physiological ReportsOpen Access

Calcium current properties in dystrophin-deficient ventricular cardiomyocytes from aged mdx mice

Q: What is the clinical evidence from this study?

Study design: Other. Population: Duchenne muscular dystrophy (DMD). Intervention: Dystrophin deficiency (mdx mouse model) vs. Wild-type (wt) mice. Primary outcome: L-type and T-type calcium current properties (current density and decay half-time).

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Key result

L-type and T-type calcium current properties and sarcoplasmic reticulum calcium release in ventricular cardiomyocytes from aged mdx mice were similar to those from aged wild-type mice.

Authors

LRLena RubiInstitute for Biomedical Engineering HTHannes TodtUniversity of Vienna HKHelmut KubistaUniversity of Vienna

Discussion

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Implication

Calcium handling is preserved in aged mdx cardiomyocytes; leaves open calcium-independent mechanisms of cardiomyopathy in dystrophy models.

PICO

Population

Ventricular cardiomyocytes isolated from male wild-type and dystrophin-deficient mdx mice aged 52 to 92 weeks to study age-related cardiac complications.

Exposure / Comparator

Dystrophin deficiency (mdx mouse model) vs Wild-type (wt) mice

Primary Outcome

L-type and T-type calcium current properties (current density and decay half-time)

Limitations

Only male mice were used in the study.
The exact mechanisms generating ECG deviations in aged mdx mice remain speculative.
In vitro findings in isolated cardiomyocytes may not fully capture in vivo cardiac electrophysiology.

Cite This Study

Rubi et al. (2018) studied Duchenne muscular dystrophy (DMD). Dystrophin deficiency (mdx mouse model) vs. Wild-type (wt) mice was evaluated on L-type and T-type calcium current properties (current density and decay half-time). L-type and T-type calcium current properties and sarcoplasmic reticulum calcium release in ventricular cardiomyocytes from aged mdx mice were similar to those from aged wild-type mice.

synapsesocial.com/papers/6a95abdcc0716d628690f926 https://doi.org/10.14814/phy2.13567

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Implication

Calcium handling is preserved in aged mdx cardiomyocytes; leaves open calcium-independent mechanisms of cardiomyopathy in dystrophy models.

Calcium current properties in dystrophin-deficient ventricular cardiomyocytes from aged mdx mice

Discussion

Member takes

Implication

PICO

Limitations

Cite This Study

Calcium current properties in dystrophin-deficient ventricular cardiomyocytes from aged mdx mice

Discussion

Member takes

Implication

PICO

Limitations

Cite This Study

Also Consider

Also Consider