Evidence map›Paper›PMID 41634115›Full record

ArticleScientific reports2026

The effect of inflammatory factors on unstable angina risk, from the gene level.

Jie Lou, QianZhen Huang, Runfeng Zhan, Qiulan Yang

Abstract read
In one paragraph

Article in Scientific 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.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Jie Lou *of Clinical Laboratory, Taicang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, No.140 renminnan road, Taicang, Jiangsu Province, China.
QianZhen Huang *of Clinical Laboratory, Taicang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, No.140 renminnan road, Taicang, Jiangsu Province, China.
Runfeng ZhanDepartment of Cardiovascular Medicine, School of Clinical Medicine, Southwest Medical University, Luzhou, 646000, Sichuan, China. stephenstewart@yeah.net.
Qiulan Yangof Clinical Laboratory, Taicang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, No.140 renminnan road, Taicang, Jiangsu Province, China. Yang18051238167@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation and its genetic regulation play crucial roles in the development of unstable angina (UA), a key manifestation of coronary artery disease (CAD). However, the genetic determinants that influence cytokine production and interindividual inflammatory responses remain incompletely understood, particularly in the Chinese population. This study aimed to clarify the relationship between inflammatory cytokine gene polymorphisms, serum cytokine expression, and UA risk. A hospital-based case-control study was conducted in 160 patients with UA and 280 age- and sex-matched healthy controls. Participants meeting the 2007 ACC/AHA UA/NSTEMI diagnostic criteria and angiographic evidence of ≥ 50% coronary stenosis were included, while individuals with systemic inflammatory or metabolic disorders were excluded. Serum cytokine levels (IL-1β, IL-6, IL-10, IL-17, IFN-γ, TNF-α) were quantified by ELISA, and 13 cytokine gene loci were genotyped using PCR-RFLP. Associations between polymorphisms and UA were evaluated using multivariate logistic regression with odds ratios (ORs) and 95% confidence intervals (CIs). All cytokines were significantly elevated in UA patients compared with controls (p < 0.01), with IL-10 showing the largest increase (3.2-fold). Polymorphisms at seven loci were significantly associated with UA susceptibility: IL-1β - 511 C/T (TT vs. CC: OR = 6.39, 95% CI 2.94-13.87), TNF-α - 308 G/A (AA vs. GG: OR = 2.56, 95% CI 1.50-4.37), IL-6 - 1363 G/T (GT vs. GG: OR = 0.52, 95% CI 0.34-0.80), IL-10 - 1082 G/A and - 592 C/A, IL-17 rs2275913, and IFN-γ + 874 A/T (all p < 0.05). ROC analysis revealed strong discriminatory ability for IL-1β - 511 C/T (AUC = 0.87) and TNF-α - 308 G/A (AUC = 0.84), both with sensitivity and specificity > 80%. Moreover, carriers of risk alleles (e.g., IL-1β T, TNF-α A) exhibited higher cytokine levels, indicating functional upregulation of inflammatory activity. Cytokine gene polymorphisms, particularly IL-1β - 511 C/T and TNF-α - 308 G/A, are associated with heightened inflammatory responses and increased UA susceptibility. These variants may serve as potential genetic biomarkers for coronary instability, though further multicenter and functional validation is warranted before clinical application. ‌Keywords‌: unstable angina; coronary artery disease; inflammatory cytokines; genetic polymorphism; biomarker; Enzyme-Linked Immunosorbent Assay; Polymerase Chain Reaction-Restriction Fragment Length Polymorphism.

Indexed as

Angina, UnstableCytokinesInflammationAgedCase-Control StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsTumor Necrosis Factor-alphaCytokinesTumor Necrosis Factor-alpha

Identifiers

PMID41634115
PMCPMC12920909

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.