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July 5, 2019Journal of EndocrinologyOpen Access

Inhibition of EGFR-STAT3 attenuates cardiomyopathy in streptozotocin-induced type 1 diabetes

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Why the study?

Elevated STAT3 activity is implicated in diabetic cardiomyopathy, and the authors hypothesized its fibrosis-promoting and hypertrophic actions are linked to activation by EGFR.

Does blockade of STAT3 or EGFR attenuate cardiomyopathy in STZ-induced type 1 diabetic mice and cultured cardiomyocytes?

Population

Cultured cardiomyocytes challenged with high-concentration glucose and streptozotocin-induced type 1 diabetic mice

Comparison

Blockade of STAT3 or EGFR using selective inhibitors S3I-201 and erlotinib or siRNAs

Authors

WLWu LuoUniversity Health NetworkLHLan Huang81th Hospital of PLAJWJingying WangCentral South University

Discussion

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Overview

Hypothesis-generating for EGFR-STAT3 targeting in diabetic cardiomyopathy; leaves open any clinical relevance or therapeutic translation.

Structured PICO

Does blockade of STAT3 or EGFR attenuate cardiomyopathy in STZ-induced type 1 diabetic mice and cultured cardiomyocytes?

P
Population
Cultured cardiomyocytes exposed to high-concentration glucose and streptozotocin (STZ)-induced type 1 diabetic mice
I
Intervention
Blockade of STAT3 or EGFR using selective inhibitors (S3I-201 and erlotinib) and siRNAs
C
Comparator
Untreated or vehicle-treated diabetic mice and cardiomyocytes (implied)
O
Outcome
Myocardial structural and functional deficits, STAT3 phosphorylation, and expression of genes regulating fibrosis and hypertrophysurrogate

Inhibition of the EGFR-STAT3 signaling axis attenuates structural and functional deficits in a mouse model of diabetic cardiomyopathy, suggesting a potential therapeutic target.

Cite This Study

Luo et al. (2019) studied this question.

synapsesocial.com/papers/6a6fbddfa7fbea1e4407d61ahttps://doi.org/10.1530/joe-19-0058
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Also Consider

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