Circular RNA circCHFR downregulation protects against oxidized low-density lipoprotein-induced endothelial injury via regulation of microRNA-15b-5p/growth arrest …

Y Li, B Wang - Bioengineered, 2022 - Taylor & Francis
Atherosclerosis is the leading cause of coronary heart disease. In recent years,
circ_0029589 (circCHFR) has been found to be associated with atherosclerosis …

Circ_0093887 regulated ox-LDL induced human aortic endothelial cells viability, apoptosis, and inflammation through modulating miR-758-3p/BAMBI axis in …

Y Wang, X Chen, Z Lu, C Lai - Clinical Hemorheology and …, 2022 - content.iospress.com
BACKGROUND: Compelling evidence demonstrated that circular RNAs (circRNAs) were
involved in the progression of atherosclerosis (AS). However, the role of circ 0093887 in the …

CircUSP36 knockdown alleviates oxidized low‑density lipoprotein‑induced cell injury and inflammatory responses in human umbilical vein endothelial cells via the …

J Miao, B Wang, R Shao… - … journal of molecular …, 2021 - spandidos-publications.com
The dysfunctions of human umbilical vein endothelial cells (HUVECs) are important features
of atherosclerosis (AS). Circular RNAs (circRNAs) are regulators of a wide range of human …

Circ-USP9X inhibition reduces oxidized low-density lipoprotein–induced endothelial cell injury via the microRNA 599/Chloride intracellular channel 4 axis

H Peng, J Sun, Y Li, Y Zhang… - Journal of Cardiovascular …, 2021 - journals.lww.com
Atherosclerosis (AS) is the common pathological basis of cardiovascular disease. Circular
RNA circ-USP9X (hsa_circ_0090231) has been discovered to be upregulated in oxidized …

[HTML][HTML] Circ_ROBO2/miR-186-5p/TRIM14 axis regulates oxidized low-density lipoprotein-induced cardiac microvascular endothelial cell injury

Q Ye, C Ju, Z Ye, J Tong - Regenerative Therapy, 2022 - Elsevier
Background Coronary artery disease (CAD) is one of the main risks of death, which is mainly
caused by coronary arteries arteriosclerosis. Circular RNAs (circRNAs) have shown …

Circ_0093887 upregulates CCND2 and SUCNR1 to inhibit the ox‐LDL‐induced endothelial dysfunction in atherosclerosis by functioning as a miR‐876‐3p sponge

Y Gao, G Li, S Fan, Y Wang, H Wei… - Clinical and …, 2021 - Wiley Online Library
Circular RNAs (circRNAs) are widely expressed in mammals and act as regulatory targets in
the atherogenesis. The objective of this study was to research the biological role and …

[PDF][PDF] Circ_CHFR expedites cell growth, migration and inflammation in ox-LDL-treated human vascular smooth muscle cells via the miR-214-3p/Wnt3/β-catenin …

JB Zhuang, T Li, XM Hu, M Ning… - European Review for …, 2020 - europeanreview.org
OBJECTIVE: Atherosclerosis (AS) is a representative inflammatory vascular disease. This
study explored the molecular pathogenesis of AS based on circular RNA (circRNA), the …

Circular RNA circ_0029589 promotes ox-LDL-induced endothelial cell injury through regulating RAB22A by serving as a sponge of miR-1197

D He, Z Li, Y Chen, M Huang - Clinical Hemorheology and …, 2023 - content.iospress.com
BACKGROUND: Dysfunction of endothelial cells is now considered a vital contributor to the
pathogenesis of atherosclerosis (AS). Moreover, circular RNA (circRNA) circ_0029589 has …

Circ_0003423 alleviates oxidized low-density lipoprotein-induced endothelial cell injury by sponging miR-142-3p and activating sirtuin 3/superoxide dismutase 2 …

P Wang, H Zhang, Y Wang - Journal of Surgical Research, 2022 - Elsevier
Introduction Atherosclerosis (AS) is a common cardiovascular disease with high morbidity
and mortality globally. Circular RNAs (circRNAs) have been shown to regulate AS …

Knockdown of circ_0002194 protects against oxidized low-density lipoprotein-induced cell damage via the regulation of the miR-637/PACS2 axis in human vascular …

R Mei, M Wu, F Ren - Interactive CardioVascular and Thoracic …, 2022 - academic.oup.com
OBJECTIVES Atherosclerosis is one of the most common cardiovascular diseases. The
functional roles of circular (circ) RNAs have been discovered in atherosclerosis. Our goal …