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细胞色素P450(CYP)1酶在急性肺损伤中的作用:从分子机制到治疗意义

Cytochrome P450 (CYP) 1 enzymes in acute lung injury: from molecular insights to therapeutic implications.

作者信息

You Yiting, Huang Jingqian, Zhu Xiaoyan, Sheng Hui, Liu Yujian

机构信息

School of Kinesiology, The Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, People's Republic of China.

Department of Physiology, Naval Medical University, Shanghai, People's Republic of China.

出版信息

Redox Rep. 2025 Dec;30(1):2550807. doi: 10.1080/13510002.2025.2550807. Epub 2025 Sep 2.

DOI:10.1080/13510002.2025.2550807
PMID:40897326
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12406335/
Abstract

OBJECTIVE

This review aims to explore the roles and mechanisms of cytochrome P450 subfamily 1 (CYP1) enzymes in acute lung injury (ALI), and to discuss their potential as therapeutic targets.

METHODS

A comprehensive literature search was conducted using PubMed and Web of Science to identify relevant studies on the involvement of CYP1 enzymes-specifically CYP1A and CYP1B1-in various forms of ALI, including hyperoxic lung injury, sepsis-associated ALI, and COVID-19 pneumonia.

RESULTS

CYP1 enzymes, induced by the aromatic hydrocarbon receptor (AhR), contribute differentially to ALI. CYP1A enzymes exhibit protective effects, whereas CYP1B1 promotes lung injury, potentially through oxidative stress-related pathways such as Nrf2, NF-κB, and MAPK signaling.

CONCLUSION

The distinct functions of CYP1 isoforms in ALI suggest their clinical relevance, highlighting the potential for isoform-specific targeting in the treatment of acute respiratory conditions.

摘要

目的

本综述旨在探讨细胞色素P450 1亚家族(CYP1)酶在急性肺损伤(ALI)中的作用和机制,并讨论它们作为治疗靶点的潜力。

方法

使用PubMed和Web of Science进行全面的文献检索,以确定关于CYP1酶(特别是CYP1A和CYP1B1)参与各种形式ALI的相关研究,包括高氧性肺损伤、脓毒症相关性ALI和新型冠状病毒肺炎。

结果

由芳烃受体(AhR)诱导的CYP1酶对ALI的作用各不相同。CYP1A酶具有保护作用,而CYP1B1则可能通过Nrf2、NF-κB和MAPK信号等氧化应激相关途径促进肺损伤。

结论

CYP1同工型在ALI中的不同功能表明它们与临床相关,突出了在急性呼吸疾病治疗中进行同工型特异性靶向治疗的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/2fe3e5d2743b/YRER_A_2550807_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/3d6987965f28/YRER_A_2550807_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/7a49dd5b2a40/YRER_A_2550807_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/56e875a61a99/YRER_A_2550807_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/2fe3e5d2743b/YRER_A_2550807_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/3d6987965f28/YRER_A_2550807_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/7a49dd5b2a40/YRER_A_2550807_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/56e875a61a99/YRER_A_2550807_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85e8/12406335/2fe3e5d2743b/YRER_A_2550807_F0004_OC.jpg

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