ArticleiScience2024
CircTMEM165 facilitates endothelial repair by modulating mitochondrial fission via miR-192/SCP2
Article in iScience, 2024. 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 It has been retracted, and should not be counted.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 5 papers.
What it found
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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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Oxidized lipids as molecular biomarkers in carotid in-stent restenosis: mechanisms and clinical implications.Frontiers in neurology · 2026Review
- tRF-AspGTC Promotes Intracranial Aneurysm Formation by Controlling TRIM29-Mediated Galectin-3 Ubiquitination.Research (Washington, D.C.) · 2025Article
- Putative role of TMEM165 in congenital cardiomyopathies.Frontiers in molecular neuroscience · 2025Review
- Mitochondrial fusion and fission in vascular disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Lactylation: An Innovative Approach to Disease Control.Aging and disease · 2024Review
Corrections and comments
- Retracted
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutive explorations indicate a correlation between circular RNAs (circRNAs) and cardiovascular diseases. However, the involvement of circRNAs in endothelial recuperation and in-stent restenosis (ISR) remains underexplored. CircTMEM165 has first been reported to be highly expressed in hypoxic human umbilical vein endothelial cells (HUVECs). Here, we identified that circTMEM165 was downregulated in ISR patients, inversely correlating with ISR severity. Functionally, circTMEM165 was found to be abundant in endothelial cells, inhibiting inflammation, and adhesion. Particularly, we first observed that circTMEM165 could alleviate HUVECs apoptosis and mitochondrial fission induced by lipopolysaccharide (LPS). Mechanistically, circTMEM165, as a miR-192-3p sponge, enhancing SCP2 expression, which serves as a critical regulator of HUVECs biological functions. Moreover,
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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 Socratic graph.