Hypoxia-induced reactive oxygen species in organ and tissue fibrosis

LINSHEN XIE; QIAOLAN WANG; JINGXUAN MA; YE ZENG

doi:10.32604/biocell.2023.024738

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Open Access

REVIEW

Hypoxia-induced reactive oxygen species in organ and tissue fibrosis

LINSHEN XIE¹, QIAOLAN WANG¹, JINGXUAN MA¹, YE ZENG^2,*
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:

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

Received 07 June 2022; Accepted 15 July 2022; Issue published 18 November 2022

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.

Keywords

Fibrosis; Oxidative stress; Hypoxia

Cite This Article

XIE, L., WANG, Q., MA, J., ZENG, Y. (2023). Hypoxia-induced reactive oxygen species in organ and tissue fibrosis. BIOCELL, 47(2), 261–267.

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