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May 19, 2023Clinical Hemorheology and Microcirculation

Silencing of circ_CHMP5 reversed ox-LDL-induced inhibition of HUVEC proliferation and angiogenesis and reduced apoptosis via the miR-516b-5p/TGFβR2 axis.

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Population

Serum from atherosclerosis patients and oxidized low-density lipoprotein-induced human umbilical vein…

Comparison

circ_CHMP5 knockdown vs ox-LDL exposure alone / control

Design

Preclinical

Key result

Silencing of circ_CHMP5 reversed ox-LDL-induced inhibition of HUVEC proliferation and angiogenesis and reduced apoptosis via the miR-516b-5p/TGFβR2 axis.

Authors

YWYueru WangPLPing LiuWYWuxiao Yang

Discussion

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Overview

circ_CHMP5 axis in endothelial injury is hypothesis-generating; leaves open validation as biomarker or target in atherosclerosis.

Structured PICO

P
Population
Serum from atherosclerosis (AS) patients and oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs)
I
Intervention
circ_CHMP5 knockdown
C
Comparator
ox-LDL exposure alone / control
O
Outcome
Cell proliferation, apoptosis, and tube formation (angiogenesis)surrogate

Knockdown of circ_CHMP5 protects endothelial cells from ox-LDL-induced damage by modulating the miR-516b-5p/TGFβR2 axis, suggesting a potential therapeutic target for atherosclerosis.

Cite This Study

Wang et al. (2023) studied Atherosclerosis. Circ_CHMP5 knockdown vs. ox-LDL-induced HUVECs without knockdown was evaluated on Cell proliferation, apoptosis, and tube formation. Silencing of circ_CHMP5 reversed ox-LDL-induced inhibition of HUVEC proliferation and angiogenesis and reduced apoptosis via the miR-516b-5p/TGFβR2 axis.

synapsesocial.com/papers/6ab9d97e2dc0fb7efdc04cbfhttps://doi.org/10.3233/ch-231722
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