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February 4, 2020Journal of Receptors and Signal Transduction

Liraglutide reduces hyperglycemia-induced cardiomyocyte death through activating glucagon-like peptide 1 receptor and targeting AMPK pathway

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Why the study?

Hyperglycemia-mediated cardiomyocyte damage is associated with inflammation and AMPK inactivation, prompting exploration of the protective effects of liraglutide on the AMPK pathway and GLP-1 receptor in diabetic cardiomyopathy.

Does liraglutide reduce hyperglycemia-induced cardiomyocyte death in an in vitro model?

Population

Cardiomyocytes exposed to high-glucose stress

Comparison

Liraglutide vs high-glucose stress alone

Design

In vitro experimental study

Authors

GMGuanqun MaYLYingwu LiuYWYu Wang

Discussion

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Overview

Liraglutide may protect high-glucose cardiomyocytes via AMPK/GLP-1R; leaves open clinical translation in diabetic cardiomyopathy.

Structured PICO

Does liraglutide reduce hyperglycemia-induced cardiomyocyte death in an in vitro model?

P
Population
Cardiomyocytes treated with high-glucose stress (in vitro model of diabetic cardiomyopathy)
I
Intervention
Liraglutide
C
Comparator
High-glucose stress without liraglutide
O
Outcome
Cardiomyocyte viability and apoptosissurrogate

Liraglutide protects cardiomyocytes from hyperglycemia-induced damage by activating the AMPK pathway and upregulating the GLP-1 receptor.

Cite This Study

Ma et al. (2020) studied this question.

synapsesocial.com/papers/6a6f9ab235aa2c282ce0f294https://doi.org/10.1080/10799893.2020.1719517
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