Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis

The lens is continuously exposed to oxidative stress insults, such as ultraviolet radiation and other oxidative factors, during the aging process. The lens possesses powerful oxidative stress defense systems to maintain its redox homeostasis, one of which employs connexin channels. Connexins are a f...

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Main Authors: Yumeng Quan, Yu Du, Yuxin Tong, Sumin Gu, Jean X. Jiang
Format: Article
Language:English
Published: MDPI AG 2021-08-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/10/9/1374
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author Yumeng Quan
Yu Du
Yuxin Tong
Sumin Gu
Jean X. Jiang
author_facet Yumeng Quan
Yu Du
Yuxin Tong
Sumin Gu
Jean X. Jiang
author_sort Yumeng Quan
collection DOAJ
description The lens is continuously exposed to oxidative stress insults, such as ultraviolet radiation and other oxidative factors, during the aging process. The lens possesses powerful oxidative stress defense systems to maintain its redox homeostasis, one of which employs connexin channels. Connexins are a family of proteins that form: (1) Hemichannels that mediate the communication between the intracellular and extracellular environments, and (2) gap junction channels that mediate cell-cell communication between adjacent cells. The avascular lens transports nutrition and metabolites through an extensive network of connexin channels, which allows the passage of small molecules, including antioxidants and oxidized wastes. Oxidative stress-induced post-translational modifications of connexins, in turn, regulates gap junction and hemichannel permeability. Recent evidence suggests that dysfunction of connexins gap junction channels and hemichannels may induce cataract formation through impaired redox homeostasis. Here, we review the recent advances in the knowledge of connexin channels in lens redox homeostasis and their response to cataract-related oxidative stress by discussing two major aspects: (1) The role of lens connexins and channels in oxidative stress and cataractogenesis, and (2) the impact and underlying mechanism of oxidative stress in regulating connexin channels.
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spelling doaj.art-373dc0f250fd43b48856e6e65bb773bf2023-11-22T11:47:47ZengMDPI AGAntioxidants2076-39212021-08-01109137410.3390/antiox10091374Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in CataractogenesisYumeng Quan0Yu Du1Yuxin Tong2Sumin Gu3Jean X. Jiang4Department of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229, USADepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229, USADepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229, USADepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229, USADepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229, USAThe lens is continuously exposed to oxidative stress insults, such as ultraviolet radiation and other oxidative factors, during the aging process. The lens possesses powerful oxidative stress defense systems to maintain its redox homeostasis, one of which employs connexin channels. Connexins are a family of proteins that form: (1) Hemichannels that mediate the communication between the intracellular and extracellular environments, and (2) gap junction channels that mediate cell-cell communication between adjacent cells. The avascular lens transports nutrition and metabolites through an extensive network of connexin channels, which allows the passage of small molecules, including antioxidants and oxidized wastes. Oxidative stress-induced post-translational modifications of connexins, in turn, regulates gap junction and hemichannel permeability. Recent evidence suggests that dysfunction of connexins gap junction channels and hemichannels may induce cataract formation through impaired redox homeostasis. Here, we review the recent advances in the knowledge of connexin channels in lens redox homeostasis and their response to cataract-related oxidative stress by discussing two major aspects: (1) The role of lens connexins and channels in oxidative stress and cataractogenesis, and (2) the impact and underlying mechanism of oxidative stress in regulating connexin channels.https://www.mdpi.com/2076-3921/10/9/1374oxidative stressconnexingap junctionhemichannellensredox homeostasis
spellingShingle Yumeng Quan
Yu Du
Yuxin Tong
Sumin Gu
Jean X. Jiang
Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis
Antioxidants
oxidative stress
connexin
gap junction
hemichannel
lens
redox homeostasis
title Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis
title_full Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis
title_fullStr Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis
title_full_unstemmed Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis
title_short Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis
title_sort connexin gap junctions and hemichannels in modulating lens redox homeostasis and oxidative stress in cataractogenesis
topic oxidative stress
connexin
gap junction
hemichannel
lens
redox homeostasis
url https://www.mdpi.com/2076-3921/10/9/1374
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