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Effects of Ferroptosis on Male Reproduction

Ferroptosis is a relatively novel form of regulated cell death that was discovered in 2012. With the increasing research related to the mechanisms of ferroptosis, previous studies have demonstrated that the inactive of the intracellular antioxidant system and iron overload can result in the accumula...

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Detalles Bibliográficos
Autores principales: Liu, Yang, Cao, Xuanhong, He, Chen, Guo, Xinrui, Cai, Hui, Aierken, Aili, Hua, Jinlian, Peng, Sha
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9267104/
https://www.ncbi.nlm.nih.gov/pubmed/35806144
http://dx.doi.org/10.3390/ijms23137139
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author Liu, Yang
Cao, Xuanhong
He, Chen
Guo, Xinrui
Cai, Hui
Aierken, Aili
Hua, Jinlian
Peng, Sha
author_facet Liu, Yang
Cao, Xuanhong
He, Chen
Guo, Xinrui
Cai, Hui
Aierken, Aili
Hua, Jinlian
Peng, Sha
author_sort Liu, Yang
collection PubMed
description Ferroptosis is a relatively novel form of regulated cell death that was discovered in 2012. With the increasing research related to the mechanisms of ferroptosis, previous studies have demonstrated that the inactive of the intracellular antioxidant system and iron overload can result in the accumulation of reactive oxygen species (ROS), which can ultimately cause lipid peroxidation in the various cell types of the body. ROS accumulation can cause sperm damage by attacking the plasma membrane and damaging DNA. Acute ferroptosis causes oxidative damage to sperm DNA and testicular oxidative stress, thereby causing male reproductive dysfunction. This review aims to discuss the metabolic network of ferroptosis, summarize and analyze the relationship between male reproductive diseases caused by iron overload as well as lipid peroxidation, and provide a novel direction for the research and prevention of various male reproductive diseases.
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spelling pubmed-92671042022-07-09 Effects of Ferroptosis on Male Reproduction Liu, Yang Cao, Xuanhong He, Chen Guo, Xinrui Cai, Hui Aierken, Aili Hua, Jinlian Peng, Sha Int J Mol Sci Review Ferroptosis is a relatively novel form of regulated cell death that was discovered in 2012. With the increasing research related to the mechanisms of ferroptosis, previous studies have demonstrated that the inactive of the intracellular antioxidant system and iron overload can result in the accumulation of reactive oxygen species (ROS), which can ultimately cause lipid peroxidation in the various cell types of the body. ROS accumulation can cause sperm damage by attacking the plasma membrane and damaging DNA. Acute ferroptosis causes oxidative damage to sperm DNA and testicular oxidative stress, thereby causing male reproductive dysfunction. This review aims to discuss the metabolic network of ferroptosis, summarize and analyze the relationship between male reproductive diseases caused by iron overload as well as lipid peroxidation, and provide a novel direction for the research and prevention of various male reproductive diseases. MDPI 2022-06-27 /pmc/articles/PMC9267104/ /pubmed/35806144 http://dx.doi.org/10.3390/ijms23137139 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Liu, Yang
Cao, Xuanhong
He, Chen
Guo, Xinrui
Cai, Hui
Aierken, Aili
Hua, Jinlian
Peng, Sha
Effects of Ferroptosis on Male Reproduction
title Effects of Ferroptosis on Male Reproduction
title_full Effects of Ferroptosis on Male Reproduction
title_fullStr Effects of Ferroptosis on Male Reproduction
title_full_unstemmed Effects of Ferroptosis on Male Reproduction
title_short Effects of Ferroptosis on Male Reproduction
title_sort effects of ferroptosis on male reproduction
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9267104/
https://www.ncbi.nlm.nih.gov/pubmed/35806144
http://dx.doi.org/10.3390/ijms23137139
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