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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MDPI AG
2021-08-01
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Series: | Antioxidants |
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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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issn | 2076-3921 |
language | English |
last_indexed | 2024-03-10T07:56:54Z |
publishDate | 2021-08-01 |
publisher | MDPI AG |
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series | Antioxidants |
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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