What is the clinical evidence from this study?

Study design: Editorial. Population: cMyBP-C deficiency. Intervention: cMyBP-C deficiency vs. Wild type. Primary outcome: Myofilament Ca2+ sensitivity.

January 10, 2006Cardiovascular ResearchOpen Access

The role of cardiac myosin binding protein-C as a regulator of myofilament Ca2+ sensitivity

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Key result

Cardiac myosin binding protein-C (cMyBP-C) actively modulates myofilament Ca2+ sensitivity, and its presence is required for PKA-induced myofilament Ca2+ desensitization.

Population

Single permeabilized ventricular myocytes from a knockout mouse model with a targeted deletion of exons 1…

Comparison

Treatment with catalytic subunit of PKA and… vs Wild type myocytes and resting sarcomere length.

Design

Editorial

Authors

HKHarald KöglerBoehringer Ingelheim (Germany)

Discussion

Member takes

Implication

cMyBP-C actively modulates myofilament Ca2+ sensitivity and is required for PKA-induced myofilament Ca2+ desensitization, which is essential for normal cardiac relaxation.

Structured PICO

Population

Single permeabilized ventricular myocytes from a knockout (KO) mouse model with a targeted deletion of exons 1 and 2 of the cMyBP-C gene, and wild type (WT) mice.

Exposure

Treatment with catalytic subunit of PKA and increase in sarcomere length (stretch to 2.3 μm).

Comparator

Wild type (WT) myocytes and resting sarcomere length (1.9 μm).

Outcome

Myofilament Ca2+ sensitivity.surrogate

cMyBP-C actively modulates myofilament Ca2+ sensitivity and is required for PKA-induced myofilament Ca2+ desensitization, which is essential for normal cardiac relaxation.

Limitations

Unclear how cTnI and cMyBP-C interact to modulate Ca2+ sensitivity in a PKA-dependent way
Discrepancies in Ca2+ sensitization across different cMyBP-C deficiency models lack a unifying theory
Potential interference from titin isoform switches on experiments investigating sarcomere length changes
Unclear how cTnI and cMyBP-C interact to modulate Ca2+ sensitivity
Discrepancies in Ca2+ sensitization across different cMyBP-C elimination models
Potential interference from titin isoform expression switch due to eccentric hypertrophy

Cite This Study

Harald Kögler (2006) conducted an editorial in cMyBP-C deficiency. cMyBP-C deficiency vs. Wild type was evaluated on Myofilament Ca2+ sensitivity. Cardiac myosin binding protein-C (cMyBP-C) actively modulates myofilament Ca2+ sensitivity, and its presence is required for PKA-induced myofilament Ca2+ desensitization.

synapsesocial.com/papers/6a9bd070dfa3a9687185044c https://doi.org/10.1016/j.cardiores.2005.12.008

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Implication

cMyBP-C actively modulates myofilament Ca2+ sensitivity and is required for PKA-induced myofilament Ca2+ desensitization, which is essential for normal cardiac relaxation.

The role of cardiac myosin binding protein-C as a regulator of myofilament Ca2+ sensitivity

Discussion

Member takes

Implication

Structured PICO

Limitations

Cite This Study

The role of cardiac myosin binding protein-C as a regulator of myofilament Ca2+ sensitivity

Discussion

Member takes

Implication

Structured PICO

Limitations

Cite This Study

Also Consider

Also Consider