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November 11, 2019Journal of Cellular Physiology

Inhibition of microRNA‐150‐5p alleviates cardiac inflammation and fibrosis via targeting Smad7 in high glucose‐treated cardiac fibroblasts

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Why the study?

Hyperglycemia-induced cardiac fibrosis is a key feature of diabetic cardiomyopathy, but the role of miR-150-5p in mediating cardiac inflammation and fibrosis in cardiac fibroblasts remained to be investigated.

Does miR-150-5p inhibition alleviate cardiac inflammation and fibrosis in high glucose-treated cardiac fibroblasts?

Population

Cardiac fibroblasts exposed to high glucose

Comparison

miR-150-5p knockdown vs miR-150-5p overexpression

Design

In vitro laboratory study

Authors

HCHui CheYWYueqiu WangYLYang Li

Discussion

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Member takes

Overview

Should not change practice in diabetic cardiomyopathy; hypothesis-generating for miR-150-5p inhibition in cardiac fibroblasts.

Structured PICO

Does miR-150-5p inhibition alleviate cardiac inflammation and fibrosis in high glucose-treated cardiac fibroblasts?

P
Population
Cardiac fibroblasts (CFs) treated with high glucose (HG)
I
Intervention
miR-150-5p knockdown/inhibition
C
Comparator
miR-150-5p overexpression and/or untreated/control CFs
O
Outcome
Cardiac inflammation (proinflammatory cytokine production IL-1β, NF-κB activity) and cardiac fibrosis (CTGF, FN, α-SMA, Col-I, Col-III)surrogate

Inhibition of miR-150-5p ameliorates high glucose-induced cardiac inflammation and fibrosis in cardiac fibroblasts by targeting Smad7, suggesting a potential therapeutic target for diabetic cardiomyopathy.

Cite This Study

Che et al. (2019) studied this question.

synapsesocial.com/papers/6a088ebe113ba5b476de454fhttps://doi.org/10.1002/jcp.29386
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