{"title":"Riboflavin and Histidine Metabolisms Are Two Key Pathways Related to the Clinically Isolated Syndrome (CIS): a WGCNA-based in silico Analysis","authors":"Mansoor Salehi, Parvaneh Tavakoli Afshar, Zohreh Taherian, Roya Bakhtiyari, Farzaneh Rami, M. Etemadifar","doi":"10.2174/1875692120666230504114225","DOIUrl":null,"url":null,"abstract":"\n\nAs an inflammatory disorder, Multiple Sclerosis (MS) causes demyelination, as well as axonal and neuronal injury in the central nervous system (CNS). Several clinical signs may be the indicators of MS among which, Clinically Isolated Syndrome (CIS) is the first symptom caused by the inflammation and demyelination of CNS. CIS is characterized by symptoms such as optic neuritis, brain stem or cerebellar syndrome, spinal cord syndrome, or sometimes cerebral hemispheric dysfunction.\n\n\n\nSo far, metabolic pathways involved in the development of CIS are not fully understood. Therefore, in this study, weighted gene co-expression network analysis (WGCNA) has been used to identify differentially expressed genes in CIS disease and the main pathways associated with it.\n\n\n\nWe grouped differentially expressed genes along with the functionally related genes into large modules to obtain their direct and indirect relationships.\n\n\n\nThe results have identified two new pathways associated with CIS, including riboflavin and histidine metabolism-involved pathways.\n\n\n\nRiboflavin and histidine metabolism-involved pathways may be considered potential therapeutic goals for CIS management in the future.\n","PeriodicalId":11056,"journal":{"name":"Current Pharmacogenomics and Personalized Medicine","volume":"4 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Pharmacogenomics and Personalized Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1875692120666230504114225","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Pharmacology, Toxicology and Pharmaceutics","Score":null,"Total":0}
引用次数: 0
Abstract
As an inflammatory disorder, Multiple Sclerosis (MS) causes demyelination, as well as axonal and neuronal injury in the central nervous system (CNS). Several clinical signs may be the indicators of MS among which, Clinically Isolated Syndrome (CIS) is the first symptom caused by the inflammation and demyelination of CNS. CIS is characterized by symptoms such as optic neuritis, brain stem or cerebellar syndrome, spinal cord syndrome, or sometimes cerebral hemispheric dysfunction.
So far, metabolic pathways involved in the development of CIS are not fully understood. Therefore, in this study, weighted gene co-expression network analysis (WGCNA) has been used to identify differentially expressed genes in CIS disease and the main pathways associated with it.
We grouped differentially expressed genes along with the functionally related genes into large modules to obtain their direct and indirect relationships.
The results have identified two new pathways associated with CIS, including riboflavin and histidine metabolism-involved pathways.
Riboflavin and histidine metabolism-involved pathways may be considered potential therapeutic goals for CIS management in the future.
期刊介绍:
Current Pharmacogenomics and Personalized Medicine (Formerly ‘Current Pharmacogenomics’) Current Pharmacogenomics and Personalized Medicine (CPPM) is an international peer reviewed biomedical journal that publishes expert reviews, and state of the art analyses on all aspects of pharmacogenomics and personalized medicine under a single cover. The CPPM addresses the complex transdisciplinary challenges and promises emerging from the fusion of knowledge domains in therapeutics and diagnostics (i.e., theragnostics). The journal bears in mind the increasingly globalized nature of health research and services.