{"title":"Nuclear Factor of Activated T Cells Signalling and Viral Pathogens: A Dynamic Cross-Talk.","authors":"Sayyad Khanizadeh, Kiana Shahzamani, Mohsen Nakhaie, Ali Pormohammad, Gholamreza Talei, Habibollah Mirzaei","doi":"10.1002/rmv.70023","DOIUrl":null,"url":null,"abstract":"<p><p>The signalling pathway of the nuclear factor of activated T cells (NFAT) plays a crucial role in regulating various cellular processes such as cardiac hypertrophy, adipose differentiation, chondrocyte development, angiogenesis, inflammation, immune system activation, organogenesis, cancer cell migration, differentiation and survival. In addition, the NFAT signalling pathway acts as a key regulator of viral infections. Accordingly, it is plausible to assume that viruses have developed different mechanisms to manipulate this pathway to promote their pathogenicity. Viral pathogens can either inhibit or upregulate NFAT signalling through various mechanisms, including modulation of calcineurin activity, calcineurin/NFAT interaction, NFAT stability and translocation, NFAT-DNA-binding activity and NFAT-transcription partner interaction. Therefore, the NFAT signalling pathway can be regarded as a promising target to control viral infections. This review discusses the dynamic interactions between the NFAT signalling pathway and viral pathogens. It also addresses several drugs and agents that can target the NFAT signalling pathway at different levels to control viral infections.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"35 2","pages":"e70023"},"PeriodicalIF":9.0000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Reviews in Medical Virology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/rmv.70023","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"VIROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
The signalling pathway of the nuclear factor of activated T cells (NFAT) plays a crucial role in regulating various cellular processes such as cardiac hypertrophy, adipose differentiation, chondrocyte development, angiogenesis, inflammation, immune system activation, organogenesis, cancer cell migration, differentiation and survival. In addition, the NFAT signalling pathway acts as a key regulator of viral infections. Accordingly, it is plausible to assume that viruses have developed different mechanisms to manipulate this pathway to promote their pathogenicity. Viral pathogens can either inhibit or upregulate NFAT signalling through various mechanisms, including modulation of calcineurin activity, calcineurin/NFAT interaction, NFAT stability and translocation, NFAT-DNA-binding activity and NFAT-transcription partner interaction. Therefore, the NFAT signalling pathway can be regarded as a promising target to control viral infections. This review discusses the dynamic interactions between the NFAT signalling pathway and viral pathogens. It also addresses several drugs and agents that can target the NFAT signalling pathway at different levels to control viral infections.
期刊介绍:
Reviews in Medical Virology aims to provide articles reviewing conceptual or technological advances in diverse areas of virology. The journal covers topics such as molecular biology, cell biology, replication, pathogenesis, immunology, immunization, epidemiology, diagnosis, treatment of viruses of medical importance, and COVID-19 research. The journal has an Impact Factor of 6.989 for the year 2020.
The readership of the journal includes clinicians, virologists, medical microbiologists, molecular biologists, infectious disease specialists, and immunologists. Reviews in Medical Virology is indexed and abstracted in databases such as CABI, Abstracts in Anthropology, ProQuest, Embase, MEDLINE/PubMed, ProQuest Central K-494, SCOPUS, and Web of Science et,al.