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Hypoxia-induced reactive oxygen species in organ and tissue fibrosis

LINSHEN XIE1, QIAOLAN WANG1, JINGXUAN MA1, YE ZENG2,*

1 West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, 610041, China
2 Institute of Biomedical Engineering, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China

* Corresponding Author: YE ZENG. Email: email

BIOCELL 2023, 47(2), 261-267. https://doi.org/10.32604/biocell.2023.024738

Abstract

Fibrosis is the end-stage change of damaged tissues in various human diseases, which can lead to permanent scarring or organ malfunction. Hypoxia leads to oxidative stress, mitochondrial dysfunction, and inflammation in dysfunctional organs and tissues. Oxidative stress resulting from the overproduction of reactive oxygen species plays a central role in the fibrosis of injured organs. This review addresses the updated knowledge of the relationship between hypoxia and tissue fibrosis mediated by the reactive oxygen species pathway. Moreover, novel anti-fibrotic strategies are discussed, which may suppress reactive oxygen species and organ fibrosis.

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APA Style
XIE, L., WANG, Q., MA, J., ZENG, Y. (2023). Hypoxia-induced reactive oxygen species in organ and tissue fibrosis. BIOCELL, 47(2), 261-267. https://doi.org/10.32604/biocell.2023.024738
Vancouver Style
XIE L, WANG Q, MA J, ZENG Y. Hypoxia-induced reactive oxygen species in organ and tissue fibrosis. BIOCELL . 2023;47(2):261-267 https://doi.org/10.32604/biocell.2023.024738
IEEE Style
L. XIE, Q. WANG, J. MA, and Y. ZENG, “Hypoxia-induced reactive oxygen species in organ and tissue fibrosis,” BIOCELL , vol. 47, no. 2, pp. 261-267, 2023. https://doi.org/10.32604/biocell.2023.024738



cc Copyright © 2023 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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