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June 7, 2018Cell Death and DiseaseOpen Access

Cardiomyocyte-specific disruption of Cathepsin K protects against doxorubicin-induced cardiotoxicity

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Why the study?

Does cardiomyocyte-specific deletion of Cathepsin K prevent doxorubicin-induced cardiotoxicity in mice?

Population

Four-month-old control and cardiomyocyte-specific Cathepsin K knockout mice

Comparison

Intraperitoneal injections of doxorubicin vs Vehicle injection

Design

Preclinical

Follow-up

1 week

Authors

RGRui GuoNankai UniversityYHYinan HuaTufts Medical CenterJRJun RenGeneral Cardiology

Discussion

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Implication

Cardiomyocyte Cathepsin K deletion attenuates doxorubicin cardiotoxicity in mice; hypothesis-generating and requires clinical validation before any therapeutic consideration.

Structured PICO

Does cardiomyocyte-specific deletion of Cathepsin K prevent doxorubicin-induced cardiotoxicity in mice?

P
Population
Four-month-old control (Myh-Cre-; Ctsk fl/fl) and cardiomyocyte-specific Cathepsin K knockout (Myh-Cre+; Ctsk fl/fl) mice
I
Intervention
Intraperitoneal injections of doxorubicin
C
Comparator
Vehicle injection
O
Outcome
Cardiac structure and function (echocardiographic properties), cardiomyocyte contractile function, and intracellular Ca2+-handling at 1 week following injectionsurrogate

Cardiomyocyte-specific deletion of Cathepsin K protects against doxorubicin-induced cardiotoxicity by attenuating apoptosis, inflammation, and metabolic disturbances, suggesting Cathepsin K as a potential therapeutic target.

Cite This Study

Guo et al. (2018) studied this question.

synapsesocial.com/papers/6a2a5075a94d6bc7baa23486https://doi.org/10.1038/s41419-018-0727-2
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