The risk of blue light exposure to human health has attracted increased research attention. Blue light, with relatively high energy, can cause irreversible photochemical damage to eye tissue. Excessive exposure of the eye to blue light tends to cause a series of alterations, such as oxidative stress, mitochondrial apoptosis, inflammatory apoptosis, mitochondrial apoptosis and DNA damage, resulting in the development of dry eye disease, glaucoma, and keratitis. Accordingly, physical protection, chemical and pharmaceutical protective measures, gene therapy, and other methods are widely used in the clinical treatment of blue light hazard. We reviewed the studies on possible blue light-induced signaling pathways and mechanisms in the eye and summarized the therapeutic approaches to addressing blue light hazard.

Myopia has become one of the most critical health problems in the world with the increasing time spent indoors and increasing close work. Pathological myopia may have multiple complications, such as myopic macular degeneration, retinal detachment, cataracts, open-angle glaucoma, and severe cases that can cause blindness. Mounting evidence suggests that the cause of myopia can be attributed to the complex interaction of environmental exposure and genetic susceptibility. An increasing number of researchers have focused on the genetic pathogenesis of myopia in recent years. Scleral remodeling and excessive axial elongating induced retina thinning and even retinal detachment are myopia's most important pathological manifestations. The related signaling pathways are indispensable in myopia occurrence and development, such as dopamine, nitric oxide, TGF-β, HIF-1α, etc. We review the current major and recent progress of biomedicine on myopia-related signaling pathways and mechanisms.

Mesenchymal stem cells and chondrocytes are an important source of the cells for cartilage tissue engineering. Therefore, the culture and expansion methods of these cells need to be improved to overcome the aging of chondrocytes and induced chondrogenic differentiation of mesenchymal stem cells. The aim of this study was to expand the cells for cartilage tissue engineering by combining the advantages of growing cells in co-culture and under a mechanically-stimulated environment. Rabbit chondrocytes and co-cultured cells (bone mesenchymal stem cells and chondrocytes) were subjected to cyclic sinusoidal dynamic tensile mechanical stimulationusing the FX-4000 tension system. Chondrocyte proliferation was assayed by flow cytometry and CFSE labeling. The cell cartilage phenotype was determined by detecting GAG, collagen II and TGF-β1 protein expression by ELISA and the Col2α1, TGF-β1 and Sox9 gene expression by RT-PCR. The results show that the co-culture improved both the proliferation ability of chondrocytes and the cartilage phenotype of co-cultured cells. A proper cyclic sinusoidal dynamic tensile mechanical stimulation improved the proliferation ability and cartilage phenotype of chondrocytes and co-cultured cells. These results suggest that the co-culture of mesenchymal stem cells with chondrocytes and proper mechanical stimulation may be an appropriate way to rapidly expand the cells that have an improved cartilage phenotype for cartilage tissue engineering.

To increase the understanding of collagen metabolism as related to scleral remodeling in the process of emmetropization and myopization. An eyelid suture that lasted 60 days was performed on one-month-old rabbits to establish an experimental monocular visual deprivation myopia model and the axial length was recorded. HE staining and transmission electron microscope were used to observe the scleral structure. The Instron 5544 was used to measure scleral elastic modulus after measuring the scleral thickness. The content of scleral tissue collagen was determined by detecting the hydroxyproline quantity and the collagen I α1, MMP-2, and TIMP-2 mRNA expression were detected by RT-PCR Kit. During regular emmetropization, the scleral collagen synthesis was higher than decomposition and the diameter of collagen fibrils increased, and then the sclera thickened and mechanical properties improved. During myopization, the scleral collagen decomposition was higher than synthesis and the diameter of collagen fibrils was smaller, and then the sclera thinner and mechanical properties lower, which resulted in a difference in scleral tissue strain. The results suggested that there were different scleral remodeling process between the emmetropization and myopization, and the collagen metabolism affected the scleral mechanical properties and scleral remodeling and then affected the scleral growth, axial elongation, and even myopization.

In recent decades, the prevalence of myopia has been on the rise globally, attributed to changes in living environments and lifestyles. This increase in myopia has become a significant public health concern. High myopia can result in thinning of the sclera and localized ectasia of the posterior sclera, which is the primary risk factor for various eye diseases and significantly impacts patients' quality of life. Therefore, it is essential to explore effective prevention strategies and programs for individuals with myopia. Collagen serves as the principal molecule in the extracellular matrix (ECM) of scleral tissue, consisting of irregular collagen fibrils. Collagen plays a crucial role in myopia progression and control. During the development of myopia, the sclera undergoes a thinning process which is primarily influenced by collagen expression decreased and remodeled, thus leading to a decrease in its biomechanical properties. Improving collagen expression and promoting collagen crosslinking can slow down the progression of myopia. In light of the above, improving collagen expression or enhancing the mechanical properties of collagen fibers via medication or surgery represents a promising approach to control myopia.