ArticleClinical hemorheology and microcirculation2023
Circ_0003575 knockdown alleviates ox-LDL-induced human aortic endothelial cell dysfunction in atherosclerosis by miR-637/TRAF6 axis.
Article in Clinical hemorheology and microcirculation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Circular RNA-mediated regulation of key signaling pathways in cardiovascular diseases: a review.Journal of advanced research · 2026Review
- Decoding the regulatory role of noncoding RNAs in biological and vascular calcification.Molecular biology reports · 2025Review
- Predictive value of miR-637 for the occurrence of myocardial hypertrophy in patients with hypertension.Journal of cardiothoracic surgery · 2025Article
Corrections and comments
- Retraction · 2025-11-23Compromised Peer Review · Concerns/Issues about Referencing/Attributions · Concerns/Issues about Third Party Involvement · Investigation by Journal/Publisher ·
- Retracted
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCircular RNAs (circRNAs) are involved in the progression of atherosclerosis (AS). The present study aimed to determine the functions and mechanism of circ_0003575 in AS.
methodsOxidized low-density lipoprotein (ox-LDL) was used to induce human aortic endothelial cells (HAECs) to establish an AS cell model. Cell Counting Kit-8 (CCK-8) assay and 5'-ethynyl-2'-deoxyuridine (EdU) assay were conducted to assess cell proliferation. Flow cytometry analysis was utilized to quantify cell apoptosis. Tube formation assay was performed to analyze angiogenesis ability. Enzyme linked immunosorbent assay (ELISA) was used to examine the concentrations of inflammatory factors. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot were manipulated for the expression of circ_0003575, microRNA-637 (miR-637) and TNF receptor associated factor 6 (TRAF6). Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were adopted to estimate the downstream targets of circ_0003575.
resultsOx-LDL treatment repressed the proliferation and angiogenesis and promoted the apoptosis and inflammation in HAECs. Circ_0003575 knockdown ameliorated ox-LDL-induced injury of HAECs. Circ_0003575 interacted with mi-R-637, which directly targeted TRAF6. Inhibition of miR-637 reversed the impacts of circ_0003575 knockdown on HAEC injury. Moreover, miR-637 overexpression promoted cell proliferation and angiogenesis and inhibited cell apoptosis and inflammation by targeting TRAF6 in ox-LDL-treated HAECs. Further, circ_0003575 silencing inhibited the activation of NF-κB pathway.
conclusionCirc_0003575 knockdown alleviated ox-LDL-induced HAEC damage by regulating miR-637/TRAF6 and NF-κB pathways.
Indexed as
Identifiers
37599528What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.