January 15, 2010Circulation ResearchOpen Access

Targeted Deletion of the Extracellular Signal-Regulated Protein Kinase 5 Attenuates Hypertrophic Response and Promotes Pressure Overload–Induced Apoptosis in the Heart

Q: What is the clinical evidence from this study?

Study design: Other. Population: Cardiac hypertrophy and hypertrophy-induced apoptosis. Intervention: Cardiomyocyte-specific deletion of the erk5 gene (ERK5(cko)) vs. Controls. Primary outcome: Hypertrophic growth, fibrosis, and apoptosis in response to hypertrophic stress.

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Key result

Cardiomyocyte-specific deletion of ERK5 in mice attenuated hypertrophic growth and fibrosis but increased apoptosis in response to hypertrophic stress.

Population

Mice with cardiomyocyte-specific deletion of the erk5 gene (ERK5) and neonatal rat cardiomyocytes subjected…

Comparison

Cardiomyocyte-specific deletion of the erk5… vs Control mice and control NRCMs

Design

Preclinical

Authors

TKTomomi KimuraYamagata University JJJiawei JinBeijing Chao-Yang Hospital MZMin ZiManchester Academic Health Science Centre

Discussion

Member takes

Implication

Dual effects of ERK5 deletion caution against inhibition; leaves open its viability as a human therapeutic target.

Structured PICO

Population

Mice with cardiomyocyte-specific deletion of the erk5 gene and neonatal rat cardiomyocytes subjected to hypertrophic stress.

Intervention

Cardiomyocyte-specific deletion of the erk5 gene (in vivo); silencing ERK5 expression or specific inhibition of its kinase activity using BIX02189 (in vitro)

Comparator

Control mice and control NRCMs

Outcome

Hypertrophic growth, fibrosis, and apoptosis in response to hypertrophic stresssurrogate

ERK5 plays a critical role in mediating cardiac hypertrophic remodeling and promoting cardiomyocyte survival under stress, likely via MEF2 regulation.

Cite This Study

Kimura et al. (2010) studied Cardiac hypertrophy and hypertrophy-induced apoptosis. Cardiomyocyte-specific deletion of the erk5 gene (ERK5(cko)) vs. Controls was evaluated on Hypertrophic growth, fibrosis, and apoptosis in response to hypertrophic stress. Cardiomyocyte-specific deletion of ERK5 in mice attenuated hypertrophic growth and fibrosis but increased apoptosis in response to hypertrophic stress.

synapsesocial.com/papers/6a93cb2c022e96156e07e262 https://doi.org/10.1161/circresaha.109.209320

Topics

Hypertension management

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Targeted Deletion of the Extracellular Signal-Regulated Protein Kinase 5 Attenuates Hypertrophic Response and Promotes Pressure Overload–Induced Apoptosis in the Heart

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

Targeted Deletion of the Extracellular Signal-Regulated Protein Kinase 5 Attenuates Hypertrophic Response and Promotes Pressure Overload–Induced Apoptosis in the Heart

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Topics

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