RESUMEN
Currently, researchers have mainly focused on the role of the tissues of the posterior segment of the eyes in the development of myopia. However, the ciliary body, an anterior ocular tissue that contracts to initiate the process of accommodation, may also play an important role in the progression of myopia due to the increased demand for near work. In the present study, we established a lens-induced myopia (LIM) animal model in guinea pigs and investigated the molecular changes in the ciliary body associated with the development of myopia based on RNA sequencing. As a result, 871 differentially expressed (DE) mRNAs and 19 DE lncRNAs were identified in the ciliary body between the LIM group and the normal control group. In addition, the lncRNA-mRNA co-expression analysis was performed to explore the target genes of lncRNAs, which were mainly enriched in the Rap1 signaling pathway, cytokine-cytokine receptor interaction, and complement and coagulation cascades pathways based on the functional enrichment analysis. Among the target genes of lncRNAs, three hub genes, including Ctnnb1, Pik3r1, and Itgb1, were found to be involved in the Rap1 signaling pathway. Interestingly, two crucial genes, Grk1 and Pde6a, which are mainly expressed in retinal photoreceptors, were enriched in visual perception in the ciliary body in functional analysis and were verified to be expressed in the ciliary body. These findings indicate the molecular pathogenetic role of the ciliary body in myopia and provide new insights into the underlying mechanism of myopia development. Further studies are needed to explore the specific contributions of these identified lncRNAs and mRNAs to the development of myopia.
Asunto(s)
Miopía , ARN Largo no Codificante , Animales , Cobayas , Cuerpo Ciliar/metabolismo , ARN Largo no Codificante/genética , ARN Mensajero/genética , ARN Mensajero/metabolismo , Visión OcularRESUMEN
Dysregulation of oxidative stress serves as a pivotal predisposing or exacerbating factor in the intricate development of numerous pathological processes and diseases. In recent years, substantial evidence has illuminated the crucial role of reactive oxygen species (ROS) in many fundamental cellular functions, including proliferation, inflammation, apoptosis, and gene expression. Notably, producing free radicals within ROS profoundly impacts a wide range of biomolecules, such as proteins and DNA, instigating cellular damage and impairing vital cellular functions. Consequently, oxidative stress emerges as a closely intertwined factor across diverse disease spectra. Remarkably, the pathogenesis of several eye diseases, including age-related macular degeneration, glaucoma, and diabetic retinopathy, manifests an intrinsic association with oxidative stress. In this comprehensive review, we briefly summarize the recent progress in elucidating the intricate role of oxidative stress in the development of ophthalmic diseases, shedding light on potential therapeutic avenues and future research directions.
Asunto(s)
Antioxidantes , Glaucoma , Humanos , Especies Reactivas de Oxígeno/metabolismo , Antioxidantes/metabolismo , Ojo/metabolismo , Estrés Oxidativo , Glaucoma/tratamiento farmacológicoRESUMEN
Myopia represents a significant public health concern worldwide, particularly affecting the ocular health of children and adolescents. The escalating prevalence of myopia in recent years underscores its urgency as a health issue among this demographic. Research indicates a profound connection between the onset of myopia, inflammatory processes and fibrosis. Individuals with inflammatory conditions like allergic conjunctivitis, choroiditis, systemic lupus erythematosus, and diabetes exhibit a heightened susceptibility to myopia. Conversely, myopic patients are at an increased risk of developing ocular inflammatory disorders, notably idiopathic multifocal choroiditis. We postulate that the expression of inflammatory markers, including NF-κB, TGF-ß, IL-1ß, IL-6, IL-8, and TNF-α, may contribute to the chronic inflammatory state observed in myopia. This paper highlights a substantial correlation between myopia and inflammation, suggesting the potential efficacy of anti-inflammatory agents in managing inflammation and slowing myopia progression.
Asunto(s)
Inflamación , Miopía , Niño , Humanos , Antiinflamatorios/uso terapéutico , Citocinas/metabolismo , Progresión de la Enfermedad , Inflamación/patología , Miopía/epidemiología , Miopía/metabolismo , Miopía/patologíaRESUMEN
In recent years, the prevalence of myopia has gradually increased, and it has become a significant global public health problem in the 21st century, posing a serious challenge to human eye health. Currently, it is confirmed that the development of myopia is attributed to the combined action of genes and environmental factors. Thus, elucidating the risk factors and pathogenesis of myopia is of great significance for the prevention and control of myopia. To elucidate the impact of gene-environment interaction on myopia, we used the Pubmed database to search for literature related to myopia. Search terms are as follows: myopia, genes, environmental factors, gene-environment interaction, and treatment. This paper reviews the effects of gene and environmental interaction on myopia.
RESUMEN
The occurrence and development of ophthalmic diseases are related to the dysfunction of eye tissues. Ubiquitin is an important form of protein post-translational modification, which plays an essential role in the occurrence and development of diseases through specific modification of target proteins. Ubiquitination governs a variety of intracellular signal transduction processes, including proteasome degradation, DNA damage repair, and cell cycle progression. Studies have found that ubiquitin can play a role in eye diseases such as cataracts, glaucoma, keratopathy, retinopathy, and eye tumors. In this paper, the role of protein ubiquitination in eye diseases was reviewed.