Evidence map›Paper›PMID 40594750›Full record

ArticleScientific reports2025

Impact of CCL5 gene polymorphisms on coronary artery disease risk and severity in the context of diabetes mellitus.

Hajer Foddha, Ikram Ben Jeddou, Hana Saoud, Saoussen Chouchene, Abdelhak Foddha, Besma Bel Haj Jrad, Hassen Ben Abdennabi, Amel Haj Khelil

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Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Review
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

8 authors.

Hajer FoddhaLaboratory of human genome and multifactorial diseases (LR12ES07), Faculty of Pharmacy, University of Monastir, BP N° 74, Street Tahar Haddad, Monastir, 5000, Tunisia. hajer.foddha@hotmail.fr.ORCID https://orcid.org/0000-0003-1490-3772
Ikram Ben JeddouLaboratory of human genome and multifactorial diseases (LR12ES07), Faculty of Pharmacy, University of Monastir, BP N° 74, Street Tahar Haddad, Monastir, 5000, Tunisia.
Hana SaoudLaboratory of Genetics, Biodiversity and Bioresource Valorization (LR11ES41), Higher Institute of Biotechnology of Monastir, University of Monastir, Monastir, Tunisia.
Saoussen ChoucheneLaboratory of human genome and multifactorial diseases (LR12ES07), Faculty of Pharmacy, University of Monastir, BP N° 74, Street Tahar Haddad, Monastir, 5000, Tunisia.
Abdelhak FoddhaCardiology Department, FattoumaBourguiba Hospital, University of Monastir, Monastir, Tunisia.
Besma Bel Haj JradLaboratory of Genetics, Biodiversity and Bioresource Valorization (LR11ES41), Higher Institute of Biotechnology of Monastir, University of Monastir, Monastir, Tunisia.
Hassen Ben AbdennabiLaboratory of human genome and multifactorial diseases (LR12ES07), Faculty of Pharmacy, University of Monastir, BP N° 74, Street Tahar Haddad, Monastir, 5000, Tunisia.
Amel Haj KhelilLaboratory of human genome and multifactorial diseases (LR12ES07), Faculty of Pharmacy, University of Monastir, BP N° 74, Street Tahar Haddad, Monastir, 5000, Tunisia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary artery disease (CAD) is a major global health burden influenced by genetic and environmental factors. Polymorphisms in the CCL5 gene, which regulates inflammatory responses, have been linked to CAD susceptibility and severity. This study examined the association of -403G/A and In1.1T/C polymorphisms in the CCL5 gene with CAD risk and severity, focusing on the role of diabetes mellitus (DM). A case-control study included 480 participants: 240 CAD patients (122 with DM and 118 without DM) and 240 healthy controls. CAD diagnosis was confirmed via coronary angiography, and severity was assessed using the Gensini score. Genotyping of -403G/A (rs2107538) and In1.1T/C (rs2280789) polymorphisms was performed using PCR-RFLP. TheA allele of -403G/A SNP was significantly associated with CAD susceptibility (p = 0.03; OR = 1.37, 95% CI: 1.03-1.82) and remained significant after adjusting for confounders. While In1.1T/C was not associated with overall CAD risk, the CC genotype correlated with higher Gensini scores, indicating greater severity (p < 0.05). Subgroup analysis showed a significant association between the C allele of In1.1T/C and CAD in diabetic patients (p = 0.009; OR = 2.06, 95% CI: 1.18-3.61) but not in non-diabetic patients. DM also strengthened the link between - 403G/A and CAD severity. These findings suggest that CCL5polymorphisms influence CAD risk and severity, with DM acting as a modifier, offering insights for personalized CAD management in diabetic populations.

Indexed as

Chemokine CCL5Coronary Artery DiseaseDiabetes MellitusGenetic Predisposition to DiseasePolymorphism, Single NucleotideAgedAllelesCase-Control StudiesFemaleGenotypeHumansMaleMiddle AgedRisk FactorsSeverity of Illness IndexCCL5 protein, humanChemokine CCL5CCL5 gene polymorphismsCoronary artery diseaseDiabetes mellitusGene–environment interactionsGenetic susceptibility

Identifiers

PMID40594750
PMCPMC12216114

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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.