Suppression of circ_0091761 ameliorates acute myocardial infarction-induced endothelial injury through regulation of miR-1278.

Authors

Bin Zhou, Haitao Wang, Kun Zhang, Jin Xie, Cuicui Yuan, Jia Jin, Jian Zhang, Meng Ma, Zhengnan Zhang

Published in

Hereditas. Volume 162. Issue 1. Pages 169. Aug 21, 2025. Epub Aug 21, 2025.

Abstract

The main objective of the article was to explore the role of circ_0091761 in acute myocardial infarction (AMI)-induced endothelial injury.
A cellular model of AMI was constructed by hypoxia-induced HUVECs. miRNAs that may interact with circ_0091761 were recognized by the ENCORI and circular RNA Interactom databases. RT-qPCR was performed to analyze the levels of circ_0091761 in AMI patients as well as miR-1278, ICAM1, and VCAM1 in hypoxia-induced HUVECs. Flow cytometry was used to detect apoptosis. ROS kit and LDH kit were used to detect the levels of ROS and LDH, respectively. Dual-luciferase reporter assay, RIP assay, and RNA pull-down assay were performed to validate their interaction between circ_0091761 and miR-1278.
circ_0091761 was elevated in AMI patients compared to healthy controls. Silencing circ_0091761 reduced apoptosis, ICAM1, and VCAM1 levels, as well as ROS and LDH. circ_0091761 could interact with miR-1278 and negatively regulate miR-1278 expression in hypoxia-induced HUVECs. At the same time, inhibiting miR-1278 reverses the protective effect of transfected si-circ_0091761 on HUVECs.
Down-regulation of circ_0091761 ameliorates AMI-induced endothelial injury by targeting miR-1278.
Not applicable.

PMID:
40835966
Bibliographic data and abstract were imported from PubMed on 21 Aug 2025.

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