Role of ferroptosis in fibrosis diseases.


Journal

The American journal of the medical sciences
ISSN: 1538-2990
Titre abrégé: Am J Med Sci
Pays: United States
ID NLM: 0370506

Informations de publication

Date de publication:
08 2023
Historique:
received: 06 09 2022
revised: 22 02 2023
accepted: 20 04 2023
medline: 7 7 2023
pubmed: 17 5 2023
entrez: 16 5 2023
Statut: ppublish

Résumé

Ferroptosis is a pervasive non-apoptotic mode of cell death that is different from autophagy or necrosis. It is mainly caused by an imbalance between the production and degradation of lipid reactive oxygen species in cells. Several metabolic pathways and biochemical processes, such as amino acid and lipid metabolism, iron handling, and mitochondrial respiration, affect and regulate cell sensitivity to peroxidation and ferroptosis. Organ fibrosis, a pathological manifestation of several etiological conditions, leads to chronic tissue injury and is characterized by excessive deposition of extracellular matrix components. Excessive tissue fibrosis can have diverse pathophysiological effects on several organ systems, eventually causing organ dysfunction and failure. The current manuscript provides a review that illustrates the link between ferroptosis and organ fibrosis and to better understand the underlying mechanisms. It provides novel potential therapeutic approaches and targets for fibrosis diseases.

Identifiants

pubmed: 37192694
pii: S0002-9629(23)01174-6
doi: 10.1016/j.amjms.2023.04.024
pii:
doi:

Substances chimiques

Iron E1UOL152H7
Reactive Oxygen Species 0

Types de publication

Journal Article Review Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

87-95

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors have no conflicts of interest.

Auteurs

Zhiyong Sun (Z)

Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China; Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, China.

Xiaozhou Zou (X)

Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China; Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, China.

Meihua Bao (M)

Hunan Key Laboratory of the Research and Development of Novel Pharmaceutical Preparations, Changsha Medical University, Changsha, China.

Zhongjie Huang (Z)

Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China; College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.

Yutao Lou (Y)

Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China; College of Pharmacy, Zhejiang University of Technology, Hangzhou, China.

Yiwen Zhang (Y)

Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China; Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, China. Electronic address: zjzyw2003@163.com.

Ping Huang (P)

Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China; Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, China. Electronic address: huangping@hmc.edu.cn.

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Classifications MeSH