November 10, 2016Journal of Cellular Biochemistry

Nrf2 Activation as a Protective Feedback to Limit Cell Death in High Glucose‐Exposed Cardiomyocytes

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Population

Cardiomyocytes in vitro and STZ-induced diabetic rat ventricles in vivo

Comparison

High glucose exposure and Nrf2 knockdown via siRNA vs Control conditions (implied)

Design

Preclinical

Authors

CTCheng‐Yen TsaiNational Taiwan University SWSu‐Ying WenUniversity of Taipei SCShi‐Yann ChengChina Medical University

Discussion

Member takes

Implication

HG-Nrf2 activation in hyperglycemia may inform diabetic cardiomyopathy mechanisms; leaves therapeutic targeting open pending in vivo data.

Structured PICO

Population

Cardiomyocytes in vitro and STZ-induced diabetic rat ventricles in vivo

Intervention

High glucose (33 mM) exposure and Nrf2 knockdown via siRNA

Comparator

Control conditions (implied)

Outcome

Nrf2 protein expression and nuclear translocation, and apoptosis markers (cleaved-caspase3, Bcl2)surrogate

High glucose induces protective Nrf2 activation in cardiomyocytes via PKCα/PKCδ-ROS-JNK/p38 signaling, suggesting a potential therapeutic target for diabetic cardiomyopathy.

Cite This Study

Tsai et al. (2016) studied this question.

synapsesocial.com/papers/6a75f9cb8d9f8f61228b76de https://doi.org/10.1002/jcb.25785

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Implication

HG-Nrf2 activation in hyperglycemia may inform diabetic cardiomyopathy mechanisms; leaves therapeutic targeting open pending in vivo data.

Nrf2 Activation as a Protective Feedback to Limit Cell Death in High Glucose‐Exposed Cardiomyocytes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Nrf2 Activation as a Protective Feedback to Limit Cell Death in High Glucose‐Exposed Cardiomyocytes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider