چاپ صفحه |  صفحه نخست سامانه |  نویسندگان |  اطلاعات تفضیلی |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده | نفر چندم مقاله |
|---|---|
| امیررضا ناصری | اول |
| مبینا اولادغفاری | دوم |
| هلیا بنده حق | سوم |
| فاطمه ملکی نژاد | چهارم |
| شهرزاد فخاری | پنجم |
| مهناز طالبی | هشتم |
| هانیه صالحی پورمهر | نهم |
| عنوان | متن |
|---|---|
| کلمات کلیدی | systematic review, multiple sclerosis, circadian rhythm regulating genes |
| خلاصه مقاله | INTRODUCTION and AIM Circadian rhythms regulating genes get into the spotlight, however, contradictory outcomes have been provided regarding their role in multiple sclerosis (MS). This study systematically explored the probable correlation between the ARNTL/BMAL-1, CLOCK, as well as PER1, PER2, and PER3 genes, and MS. METHODS Following the PRISMA statement [1], a systematic search was conducted through PubMed, Scopus, Embase, and Web of Science databases for studies published until July 2023. Clinical studies concerning the role of circadian genes in MS were considered for inclusion. The risk of bias in the included studies was assessed using the JBI critical appraisal tools and comprehensive meta-analysis (CMA4) was utilized for the quantitative synthesis. RESULTS The initial database searches provided a total of 1069 citations, of which 594 records remained after removing duplicate studies. Then, 586 studies were excluded in the title/abstract stage, leaving eight studies in which three studies were excluded because of investigation of other genes [2-4]. Finally, five studies were included in the current systematic review [5-9], and four of them were included in the quantitative synthesis. The PRISMA flow diagram regarding the study selection process is illustrated in Figure 1. Based on findings from four studies, no significant statistical difference was found between MS patients and the control groups regarding the rs6811520 single nucleotide polymorphisms(SNP) of CLOCK gene (CC: I2: 82.15%, p-value for heterogeneity<0.001; OR: 0.90; 95%CI: 0.59-1.37; p-value: 0.62; CT: I2: 82.05%, p-value for heterogeneity<0.001; OR: 1.61; 0.78-1.72; p-value: 0.46; TT: I2: 32.16%, p-value for heterogeneity: 0.219; OR:0.97; 0.82-1.15; p-value: 0.15); however, regarding the rs3789327 SNP in ARNTL/BMAL-1, a higher prevalence of CC genotype in MS patients was evident (CC: I2: 82.37%, p-value for heterogeneity: 0.017; OR: 1.38; 95%CI: 0.95-2.03; p-value: 0.09; CT: I2: 75.01%, p-value for heterogeneity: 0.045; OR: 0.89; 95%CI: 0.68-1.18; p-value: 0.42; TT: I2: 00.00%, p-value for heterogeneity: 0.88; OR: 0.86; 95%CI: 0.74-1.00; p-value: 0.05). Also, association between these genes and disease phenotype is suggested. Variable number tandem-repeat polymorphism of the PER3 gene was also reported to accelerate disease progression in individuals predisposed to MS. CONCLUSIONS This study found no role for any genotypic distribution of rs6811520 polymorphism of the CLOCK gene in MS pathgensis. CC genotype of rs3789327 SNP in ARNTL/BMAL-1 is suggestes as a genetic risk factor for MS, however, considering the limitations such as the small number of included studies, there is need for future studies on this topic. |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| P302.pdf | 1404/09/27 | 214299 | دانلود |
| CLOCK.pdf | 1404/10/17 | 10960628 | دانلود |
