Chief Supervisor

Prof. PAN Feng

Project Title

Synopsis

The prevalence of myopia is increasing worldwide. Animal studies have shown that hyperopic defocus can promote axial elongation, while myopic defocus can inhibit this process. However, the molecular mechanisms underlying this process are not yet fully understood. Electrical synapses—also known as gap junctions—are formed between the adjacent membranes of neighboring cells, with each hemichannel, or connexon, consisting of 6 connexin protein subunits. Gap junctions are widely distributed throughout the retina and play a crucial role in facilitating intercellular communication among various retinal cell types. It is currently unclear which specific types among the numerous gap junctions and connexins are primarily responsible for regulating myopia progression. Some studies suggest that peripheral myopic defocus lenses may inhibit myopia progression by upregulating the ON pathway in the retina, a process potentially mediated by gap junctions between AII amacrine cells and ON-cone bipolar cells, which are composed of connexin 36 and 45. This study aims to address the gap in knowledge by examining the role of these gap junctions in retinal signal and their potential impact on myopia progression.