Evidence map›Paper›PMID 42402508›Full record

ArticleImmunogenetics2026

Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.

Alishba Kainat, Fazlul Aziz Mian, Muhammad Asif Nawaz Khan, Mubeen Tabish Nasim, Syed Muhammad Nurulain, Nazia Bibi, Syed Tahir Abbas Shah, Muhammad Jadoon Khan, Sabir Hussain

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Article in Immunogenetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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9 authors.

Alishba KainatDepartment of Biosciences, COMSATS University Islamabad, Islamabad, 45550, Pakistan.
Fazlul Aziz MianDepartment of Cardiology, Pakistan Institute of Medical Sciences (PIMS), Islamabad, 46000, Pakistan.
Muhammad Asif Nawaz KhanDepartment of Cardiology, Pakistan Institute of Medical Sciences (PIMS), Islamabad, 46000, Pakistan.
Mubeen Tabish NasimDepartment of Biosciences, COMSATS University Islamabad, Islamabad, 45550, Pakistan.
Syed Muhammad NurulainDepartment of Biosciences, Grand Asian University, Sialkot, 7-KM, Pasroor Road, Sialkot, Pakistan.
Nazia BibiDepartment of Biosciences, COMSATS University Islamabad, Islamabad, 45550, Pakistan.
Syed Tahir Abbas ShahDepartment of Biosciences, COMSATS University Islamabad, Islamabad, 45550, Pakistan.
Muhammad Jadoon KhanDepartment of Biosciences, COMSATS University Islamabad, Islamabad, 45550, Pakistan.
Sabir HussainDepartment of Biosciences, COMSATS University Islamabad, Islamabad, 45550, Pakistan. sabirhussain@comsats.edu.pk.

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6 · The paper itself

Abstract

Cytokines are crucial in regulating hypertension and vascular inflammation. The clinical significance of circulating IL-36γ levels and IL36G gene variants in relation to essential hypertension risk was assessed because IL-36γ has been associated with several cardiovascular diseases, while its role in essential hypertension is still unknown. Serum IL-36γ levels were determined by enzyme-linked immunosorbent assay, while IL36G polymorphisms were assessed by PCR-RFLP method in 264 patients with essential hypertension and 264 normotensive controls. Patients showed significantly elevated serum IL-36γ levels (p < 0.0001) when compared with the controls. Significant association between IL36G rs11690399 and rs11683399 polymorphisms and essential hypertension susceptibility were found through genotyping analysis, with combination genotypes (GT + TT) and (TG + GG) conferring an elevated risk of a disease. A 2.6-fold and a 1.9-fold increased risk of essential hypertension was observed to the T allele of rs11690399 and the G allele of rs11683399, respectively. Significantly higher levels of IL-36γ were associated with variant genotypes, suggesting a genotype-phenotype correlation. T-T and T-G were found to be a risk haplotype for essential hypertension by haplotype analysis. A causal relationship between increased IL-36γ and the risk of hypertension was shown by Mendelian randomization (OR = 1.0066; 95% CI: 1.0028-1.0104, p < 0.0001). A diagnostic performance for IL-36γ (AUC = 0.862) was found by ROC analysis, indicating its potential as a clinical biomarker. In conclusion, there is a significant association between essential hypertension and higher IL-36γ levels and IL36G polymorphisms. These results suggest that elevated circulatory IL-36γ may play a role in the pathophysiology of essential hypertension.

Indexed as

Genetic Predisposition to DiseaseHypertensionInterleukin-1Polymorphism, Single NucleotideAdultCase-Control StudiesEssential HypertensionFemaleGenetic Association StudiesGenotypeHaplotypesHumansMaleMiddle AgedRisk FactorsIL36G protein, humanInterleukin-1AssociationEssential HypertensionGenotypingIL-36Polymorphism

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