Knowledge discovery in genetics of diabetes in Iran, a roadmap for future researches

2型糖尿病 全基因组关联研究 斯科普斯 医学 疾病 糖尿病 生物信息学 梅德林 遗传学 生物 单核苷酸多态性 内科学 基因 基因型 生物化学 内分泌学
作者
Saeed Ebrahimi Fana,Fariba Esmaeili,Shahnaz Esmaeili,Fatemeh Bandaryan,Ensieh Nasli Esfahani,Mahsa M. Amoli,Farideh Razi
标识
DOI:10.1007/s40200-021-00838-8
摘要

The pathogenesis of diabetes is considered polygenic as a result of complex interactions between genetic/epigenetic and environmental factors. This review intended to evaluate the scientometric and knowledge gap of diabetes genetics researches conducted in Iran as a case of developing countries, and drawn up a roadmap for future studies.We searched Scopus and PubMed databases from January 2015 until December 2019 using the keywords: (diabetes OR diabetic) AND (Iran). All publications were reviewed by two experts and after choosing relevant articles, they were categorized based on the subject, level of evidence, study design, publication year, and type of genetic studies.Of 10,540 records, 428 articles were met the inclusion criteria. Generally, the number of researches about diabetes genetics rose since 2015. Case-control/cross-sectional and animal studies were the common types of study design and based on the subject, the most frequent researches were about genetic factors involved in diabetes development (38%). Briefly, the top seven genes that were evaluated for T2DM were TCF7L2, APOAII, FTO, PON1, ADIPOQ, MTHFR, and PPARG respectively, and also, CTL4 for T1DM. miR-21, miR-155, and miR-375 respectively were the most micro-RNAs that were evaluated. Furthermore, there were six studies about lncRNAs.Investigation about the genetic of diabetes is progressed although there are some limitations like non-homogenous data from Iran, heterogeneity of ethnicity, and rationale of studies. Compared to the previous analysis in Iran, still, GWAS and large-scale studies are required to achieve better policies for manage and control of diabetes disease.The online version contains supplementary material available at 10.1007/s40200-021-00838-8.

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