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Nrf2 通路在病毒呼吸道感染导致的气道组织损伤中的作用。

The Role of the Nrf2 Pathway in Airway Tissue Damage Due to Viral Respiratory Infections.

机构信息

Division of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

Division of Infectious Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.

出版信息

Int J Mol Sci. 2024 Jun 27;25(13):7042. doi: 10.3390/ijms25137042.

DOI:10.3390/ijms25137042
PMID:39000157
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11241721/
Abstract

Respiratory viruses constitute a significant cause of illness and death worldwide. Respiratory virus-associated injuries include oxidative stress, ferroptosis, inflammation, pyroptosis, apoptosis, fibrosis, autoimmunity, and vascular injury. Several studies have demonstrated the involvement of the nuclear factor erythroid 2-related factor 2 (Nrf2) in the pathophysiology of viral infection and associated complications. It has thus emerged as a pivotal player in cellular defense mechanisms against such damage. Here, we discuss the impact of Nrf2 activation on airway injuries induced by respiratory viruses, including viruses, coronaviruses, rhinoviruses, and respiratory syncytial viruses. The inhibition or deregulation of Nrf2 pathway activation induces airway tissue damage in the presence of viral respiratory infections. In contrast, Nrf2 pathway activation demonstrates protection against tissue and organ injuries. Clinical trials involving Nrf2 agonists are needed to define the effect of Nrf2 therapeutics on airway tissues and organs damaged by viral respiratory infections.

摘要

呼吸道病毒是导致全球疾病和死亡的重要原因。与呼吸道病毒相关的损伤包括氧化应激、铁死亡、炎症、细胞焦亡、细胞凋亡、纤维化、自身免疫和血管损伤。多项研究表明,核因子红细胞 2 相关因子 2(Nrf2)参与病毒感染及其相关并发症的病理生理学过程。因此,它成为细胞防御机制对抗此类损伤的关键因素。在这里,我们讨论了 Nrf2 激活对呼吸道病毒(包括病毒、冠状病毒、鼻病毒和呼吸道合胞病毒)引起的气道损伤的影响。在存在病毒呼吸道感染的情况下,Nrf2 通路激活的抑制或失调会导致气道组织损伤。相反,Nrf2 通路的激活显示出对组织和器官损伤的保护作用。需要进行涉及 Nrf2 激动剂的临床试验,以确定 Nrf2 治疗药物对病毒呼吸道感染损伤的气道组织和器官的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/1e65c0a11f3c/ijms-25-07042-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/10a404bfabc0/ijms-25-07042-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/92973304a9bf/ijms-25-07042-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/b87c369ac3ba/ijms-25-07042-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/1e65c0a11f3c/ijms-25-07042-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/10a404bfabc0/ijms-25-07042-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/92973304a9bf/ijms-25-07042-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/b87c369ac3ba/ijms-25-07042-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28cd/11241721/1e65c0a11f3c/ijms-25-07042-g004.jpg

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