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A Study on Associations of Long Noncoding RNA HOTAIR Polymorphisms With Genetic Susceptibility to Chronic Kidney Disease

Overview
Journal J Clin Lab Anal
Publisher Wiley
Date 2024 Jul 3
PMID 38958113
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Abstract

Background: The importance of long noncoding RNAs (lncRNAs) in various biological processes has been increasingly recognized in recent years. This study investigated how gene polymorphism in HOX transcript antisense RNA (HOTAIR) lncRNA affects the predisposition to chronic kidney disease (CKD).

Methods: This study comprised 150 patients with CKD and 150 healthy controls. A PCR-RFLP and ARMS-PCR techniques were used for genotyping the five target polymorphisms.

Results: According to our findings, rs4759314 confers strong protection against CKD in allelic, dominant, and codominant heterozygote genetic patterns. Furthermore, rs3816153 decreased CKD risk by 78% when TT versus GG, 55% when GG+GT versus TT, and 74% when GT versus TT+GG. In contrast, the CC+CT genotype [odds ratio (OR) = 1.66, 95% confidence intervals (CIs) = 1.05-2.63] and the T allele (OR = 1.50, 95% CI = 1.06-2.11) of rs12826786, as well as the TT genotype (OR = 2.52, 95% CI = 1.06-5.98) of rs3816153 markedly increased the risk of CKD in the Iranian population. Although no linkage disequilibrium was found between the studied variants, the CTGGG haplotype was associated with a decreased risk of CKD by 86% (OR = 0.14, 95% CI = 0.03-0.66).

Conclusion: The rs920778 was not correlated with CKD risk, whereas the HOTAIR rs4759314, rs12826786, rs1899663, and rs3816153 polymorphisms affected the risk of CKD in our population. It seems essential to conduct repeated studies across various ethnic groups to explore the link between HOTAIR variants and their impact on the disease outcome.

Citing Articles

Chronic Kidney Disease of Unknown Etiology: A Global Health Threat in Rural Agricultural Communities-Prevalence, Suspected Causes, Mechanisms, and Prevention Strategies.

Ben Khadda Z, Lahmamsi H, El Karmoudi Y, Ezrari S, El Hanafi L, Houssaini T Pathophysiology. 2024; 31(4):761-786.

PMID: 39728687 PMC: 11677577. DOI: 10.3390/pathophysiology31040052.

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