ArticleMolecular biology reports2026
Association between miRNAs and DEFA4 in coronary artery disease.
Article in Molecular biology reports, 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
backgroundCoronary artery disease (CAD) is a leading cause of death worldwide, caused by environmental factors and characterized by the formation of atherosclerotic plaques. Identification of novel biomarkers is essential for early diagnosis and risk stratification. This study aimed to investigate the expression of DEFA4 and its associated microRNAs in CAD patients and their association with demographic, clinical, and laboratory parameters.
methodsIn this case-control study, 60 CAD patients and 60 healthy controls aged 30 to 75 years were studied to evaluate the expression levels of DEFA4 and related miRNAs in peripheral blood mononuclear cells using real-time PCR. Clinical data, classical risk factors, and laboratory parameters were recorded and statistical analyses were performed using SPSS version 26.
resultsDEFA4 expression was increased in CAD patients (3.44 ± 1.36 vs.1.00 ± 0.59), especially in patients with unstable plaques (3.71 ± 1.32) compared to those with stable plaques (2.07 ± 0.40, P < 0.0001). Conversely, the expression of miR-651-5p (0.33 ± 0.13 vs. 1.00 ± 0.72), miR-8080 (0.36 ± 0.39 vs. 1.00 ± 0.35), miR-330-3p (0.55 ± 0.35 vs. 1.00 ± 0.94), miR-298 (0.36 ± 0.39 vs. 1.00 ± 0.53) were significantly decreased. DEFA4 showed a positive correlation with cholesterol (r = 0.821) and neutrophil-lymphocyte ratio (NLR) (r = 0.400), and a negative correlation with hemoglobin (r=-0.855), triglycerides (r=-0.827), and hematocrit (r=-0.850). Bioinformatics analysis through TargetScan and miRDB showed that the target sequences of the studied miRNAs on the 3'UTR region of DEFA4 have high conservation and strong context + scores validating the regulatory hypothesis. However, these strong correlations require external validation in independent cohorts.
conclusionThere is an association between increased DEFA4 expression and decreased miRNAs associated with inflammatory markers in CAD patients. However, the case and control groups were not matched for major cardiovascular risk factors, our sample size was limited, and we lacked functional validation. Therefore, these findings indicate an association rather than causation.
Indexed as
Identifiers
42377700What Socratic 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 Socratic graph.