Scholarlink

<p>Nuclear factor erythroid 2-related factor 2 (NRF2) is a central regulator of redox balance and innate antiviral defense. Because many viruses induce oxidative stress to support replication or evade immunity, understanding how NRF2 responds to infection is essential for identifying new therapeutic strategies. Current evidence shows that viral pathogens, ranging from respiratory viruses to hepatic, neurotropic, and retroviral infections, differentially manipulate the NRF2-Keap1 pathway. NRF2 activation can suppress viral replication, reduce oxidative damage, and limit inflammation, while certain viruses inhibit NRF2 to promote immune evasion or chronic disease. We also highlight situations in which persistent NRF2 activation supports cell survival and contributes to virus-associated carcinogenesis. We also demonstrate that NRF2-activating compounds such as sulforaphane, dimethyl fumarate, and 4-octyl-itaconate can modulate antiviral and anti-inflammatory responses. These insights identify NRF2 as a promising target for host-directed antiviral therapy. Disease-specific NRF2 activation or inhibition may enhance treatment efficacy, reduce tissue injury, and mitigate long-term complications. Therefore, understanding how viruses exploit or suppress NRF2 provides a basis for developing selective NRF2 modulators with translational potential for managing acute and chronic viral infections.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Nuclear factor erythroid 2-related factor: potential use as a therapeutic strategy for viral infections

  • 期刊论文

  • 发表日期：

    2026年1月21日

查看全文
  • Sama Akbarzadeh,
  • Javad Arabpour,
  • Zahra Yekanipour,
  • Nima Afshar Moghaddam,
  • Omid Gholizadeh

摘要

Nuclear factor erythroid 2-related factor 2 (NRF2) is a central regulator of redox balance and innate antiviral defense. Because many viruses induce oxidative stress to support replication or evade immunity, understanding how NRF2 responds to infection is essential for identifying new therapeutic strategies. Current evidence shows that viral pathogens, ranging from respiratory viruses to hepatic, neurotropic, and retroviral infections, differentially manipulate the NRF2-Keap1 pathway. NRF2 activation can suppress viral replication, reduce oxidative damage, and limit inflammation, while certain viruses inhibit NRF2 to promote immune evasion or chronic disease. We also highlight situations in which persistent NRF2 activation supports cell survival and contributes to virus-associated carcinogenesis. We also demonstrate that NRF2-activating compounds such as sulforaphane, dimethyl fumarate, and 4-octyl-itaconate can modulate antiviral and anti-inflammatory responses. These insights identify NRF2 as a promising target for host-directed antiviral therapy. Disease-specific NRF2 activation or inhibition may enhance treatment efficacy, reduce tissue injury, and mitigate long-term complications. Therefore, understanding how viruses exploit or suppress NRF2 provides a basis for developing selective NRF2 modulators with translational potential for managing acute and chronic viral infections.