ArticleCardiovascular drugs and therapy2026
Circulating Circ_0089762 Predicts Adverse Outcomes in Acute Myocardial Infarction Via Regulating miR‑938/STAT3‑Mediated Endothelial Dysfunction.
Article in Cardiovascular drugs and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndothelial dysfunction is the initiating factor in atherosclerosis and is a persistent feature throughout the entire course of acute myocardial infarction (AMI). Circular RNA (circRNA) fulfils a vital regulatory role in cardiovascular diseases, including AMI.
aimTo investigate the expression and clinical significance of circ_0089762 in AMI, and to elucidate the molecular mechanism in regulating hypoxia/reoxygenation (H/R)-induced damage in human umbilical vein endothelial cells (HUVECs).
methodsSerum levels of circ_0089762, miR-938, and STAT3 were measured by RT-qPCR. A model H/R injury model was established in HUVECs, and by transfecting to modulate circ_0089762, miR-938, assess cell viability, apoptosis, migration, oxidative stress, and inflammation levels. The targeting relationship was validated using dual-luciferase assays. Rescue experiments were conducted to verify the regulatory axis.
resultscirc_0089762 is hyper-expressed in AMI, and it has certain diagnostic accuracy in distinguishing AMI patients from healthy individuals, as well as being associated with major adverse cardiovascular events (MACE). H/R treatment can upregulate circ_0089762 expression. Silencing circ_0089762 enhances cell viability, inhibits apoptosis, improves migration, and reduces MDA levels whilst increasing NO and SOD levels, and suppresses the release of inflammatory factors. circ_0089762 directly targets miR-938, and miR-938 directly targets STAT3. Inhibition of miR-938 reverses the protective effects of circ_0089762 knockdown, and further knockdown of STAT3 restores the endothelial protective effects.
conclusioncirc_0089762 exacerbates H/R-induced apoptosis, oxidative stress, and inflammatory response in HUVECs by regulating miR-938 and STAT3 expression. circ_0089762 may act as a potential biomarker for the diagnosis, prognostic assessment, and targeted treatment of AMI.
Indexed as
Identifiers
42518073What 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.