About this Research Topic
Of the five traditional special senses (sight, hearing, touch, smell, and taste), sight is often considered the most important, and loss of vision or sight is one of the greatest human fears. The eye plays a pivotal role in helping us connect with the world. One family of proteins known as gap junctions (including connexins, pannexins, or innexins) are expressed in the different parts of the eyes and also play an essential role in maintaining the homeostasis of cells in the eye. In addition, mutations in some gap junction genes, which are called connexins, are associated with human eye diseases, such as congenital cataracts, glaucoma, myopia, and corneal and retinal diseases. However, our current knowledge of gap junctions on ocular diseases is still limited: genes and eye development, cell differentiation, and homeostasis, and how mutations in gap junction genes cause human eye diseases or change gene expressions in gap junctions in some human eye disease conditions.
To discover new methods of diagnosis and treatment of diseases based on the discovery of various pathogenic mechanisms, direct modulators and antisense technologies have been used to investigate the effects of manipulating gap junctions, with a number of achievements in pre-clinical illness models. Gap junction proteins are becoming appealing therapeutic targets because of their potential to control immunological responses, cell migration, differentiation, apoptosis, and tumorigenesis. Investigating the gap junction protein pathways may be useful in discovering more accurate prognostic indicators. Growing interest has been shown in recent years in the usage of gap junction modulators in various therapeutic settings and the particular function of connexins in various physiological and pathological states. Interventions can also be used by regulating the synthesis, transport, assembly, phosphorylation, and degradation of gap junction proteins and altering their function. Also, pre-clinical models will continue to offer a platform for these studies and the development of innovative therapeutic agents for future clinical applications. For instance, gene therapy has been demonstrated to augment or restore gap junction intercellular communication in transfected cells or knock-in mice.
In this context, the novel elucidation of the pathogenic mechanisms of eye diseases and the presentation of discoveries are essential to leading research on disease treatment. Therefore, taking advantage of the newly developed state-of-the-art technologies that target the gap junctions in the eyes may offer promise in the diagnosis and treatment of eye diseases: such as 3D organoids, stem cells, CRISPR gene therapy, gene knockout and knockin, Cryo-EM, high-efficiency gene transfection and virus-mediated gene transduction, optogenetics, combined with the unique immune-privileged eye.
This Research Topic concentrates on the following aspects of original research, review summaries, general commentary, and editorials on diagnosing and treating eye diseases.
• Gap Junction (GJ) and ocular inflammation
• GJ and ocular stem cells
• GJ and glaucoma, myopia, retinopathy, corneal diseases, posterior capsule opacification (PCO), various cataracts (congenital cataract, senile cataract, metabolic cataract, etc.), diabetic eye diseases, genetic eye diseases, etc.
To discover new methods of diagnosis and treatment of diseases based on the discovery of various pathogenic mechanisms, direct modulators and antisense technologies have been used to investigate the effects of manipulating gap junctions, with a number of achievements in pre-clinical illness models. Gap junction proteins are becoming appealing therapeutic targets because of their potential to control immunological responses, cell migration, differentiation, apoptosis, and tumorigenesis. Investigating the gap junction protein pathways may be useful in discovering more accurate prognostic indicators. Growing interest has been shown in recent years in the usage of gap junction modulators in various therapeutic settings and the particular function of connexins in various physiological and pathological states. Interventions can also be used by regulating the synthesis, transport, assembly, phosphorylation, and degradation of gap junction proteins and altering their function. Also, pre-clinical models will continue to offer a platform for these studies and the development of innovative therapeutic agents for future clinical applications. For instance, gene therapy has been demonstrated to augment or restore gap junction intercellular communication in transfected cells or knock-in mice.
In this context, the novel elucidation of the pathogenic mechanisms of eye diseases and the presentation of discoveries are essential to leading research on disease treatment. Therefore, taking advantage of the newly developed state-of-the-art technologies that target the gap junctions in the eyes may offer promise in the diagnosis and treatment of eye diseases: such as 3D organoids, stem cells, CRISPR gene therapy, gene knockout and knockin, Cryo-EM, high-efficiency gene transfection and virus-mediated gene transduction, optogenetics, combined with the unique immune-privileged eye.
This Research Topic concentrates on the following aspects of original research, review summaries, general commentary, and editorials on diagnosing and treating eye diseases.
• Gap Junction (GJ) and ocular inflammation
• GJ and ocular stem cells
• GJ and glaucoma, myopia, retinopathy, corneal diseases, posterior capsule opacification (PCO), various cataracts (congenital cataract, senile cataract, metabolic cataract, etc.), diabetic eye diseases, genetic eye diseases, etc.
Keywords: Gap junctions, eye development, mutation, hemichannels, neuromodulation, connexins, myopia, lens, cataract, glaucoma, retinopathy, retina, retinal disease
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