Abstract
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.
Highlights
The lens is an avascular and transparent organ in the anterior segment of the eye.Its primary function is to transmit and focus light onto the retina
The oxidative-induced alterations of connexin proteins decrease gap junction intercellular communication (GJIC), leading to the accumulation of oxidants and cataract formation, since antioxidant molecules cannot be delivered into the lens core
The oxidative stress on lens proteins, lipids, and DNA may result in an imbalanced redox environment and activation of signaling pathways that induce post-translational modifications of connexins and oxidation of connexin molecules
Summary
The lens is an avascular and transparent organ in the anterior segment of the eye. Its primary function is to transmit and focus light onto the retina. To maintain redox homeostasis under continuous oxidative insults, the lens develops an oxidative stress defense mechanism with powerful capacities to modulate redox metabolism. This complex antioxidative mechanism includes simple ROS scavengers and more advanced enzyme protective systems [3,4]. An internal lens microcirculation system composed of connexin channels, ion channels, and ion pumps mediates the transport of nutrition and metabolites. It plays a critical role in protecting the lens against oxidative damage [5]. We aim to provide a summary of recent research advances in our understanding of mechanical roles of connexin channels in lens redox homeostasis and oxidative stress-induced lens disorders
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
