ArticleBiochemical genetics2026
miR-203 Alleviates Myocardial Damage Caused by Acute Coronary Syndrome by Inhibiting CA125.
Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Circulating exosomal miRNA in acute coronary syndrome: mechanisms, clinical relevance and future directions.Frontiers in molecular biosciences · 2026Review
- Upregulation of Serum miRNA-3615 Serves as a Biomarker to Predict Disease Onset and Prognosis in Acute Coronary Syndrome Patients.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute coronary syndrome (ACS) is a significant contributor to cardiovascular mortality. Research has indicated that CA125 levels are linked to cardiovascular disease. This study aimed to explore the role of CA125 in ACS and its underlying mechanism. A retrospective study was conducted involving 34 healthy volunteers and 46 patients diagnosed with ACS. Clinical characteristics and CA125 expression were recorded and detected. Bioinformatics analysis was performed to identify miRNAs that regulate CA125. HL-1 cardiac muscle cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to investigate the role of CA125 in myocardial injury. An ACS mice model was constructed to further explore the role of CA125 on ACS. The levels of serum creatinine, blood urea nitrogen, uric acid, high-sensitivity C-reactive protein, cystatin C, and white blood cells in ACS were markedly higher than those in healthy volunteers. CA125 was up-regulated in ACS and was a target of miR-203. Injection of miR-203 agomir reduced plaque deposition and vascular thrombosis in the coronary lumen, alleviating myocardial damage. Additionally, miR-203 inhibited myocardial apoptosis and inflammation responses induced by OGD/R and ACS. miR-203 can reduce the inflammatory response by inhibiting CA125 expression, thereby improving ACS symptoms and mitigating ACS-induced myocardial injury.
Indexed as
Identifiers
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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.