Keratoconus (KC) is a progressive ocular disorder marked by structural and functional alterations of the cornea, leading to significant visual impairment. Recent studies indicate that these corneal changes are linked to molecular and cellular mechanisms that disrupt and degrade the extracellular matrix. This degradation is influenced by proteinases that contribute to a loss of homeostasis and an imbalance in the antioxidant/oxidative state within the cornea, fostering oxidative stress, inflammation, and apoptosis. Although these biological processes have been identified primarily through molecular biology research, omics technologies have significantly advanced our understanding of the physiological and pathological phenomena associated with KC. Omics studies encompassing genomics, transcriptomics, proteomics, epigenomics, and metabolomics, have emerged as critical tools in elucidating the complex biological landscape of various diseases, including ocular conditions. The integrative application of these studies has demonstrated their potential in personalizing medicine across diverse fields such as oncology, neurology, and ophthalmology. This review aims to describe findings from omics research applied to keratoconus, highlighting the genomic, transcriptomic, proteomic, epigenomic, and metabolomic aspects derived from ocular and other biological samples. Notably, the molecular insights gained from these studies hold promise for identifying biomarkers of keratoconus, which could enhance diagnostic accuracy and therapeutic strategies. The exploration of these biomarkers may facilitate improved management and treatment options for patients, contributing to personalized care in keratoconus management.

Glaucoma is traditionally defined as an ocular disease characterized by progressive retinal ganglion cell degeneration, in some cases with elevated intraocular pressure (IOP), and optic nerve damage. However, growing evidence indicates that glaucoma shares critical features with neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases. This study aimed to explore the systemic nature of primary open-angle glaucoma (POAG) by integrating visual function, cognitive performance, and transcriptomic profiling. We conducted a multidimensional assessment of POAG patients and age-matched controls, accounting for demographic factors. Structural parameters included retinal nerve fiber layer (RNFL) thickness, measured using optical coherence tomography (OCT), and visual field indices mean deviation (MD) and pattern standard deviation (PSD). Cognitive function was evaluated across multiple domains, encompassing visual memory, executive function, processing speed, and verbal fluency. Additionally, transcriptomic analysis was performed from conjunctival samples to identify differentially expressed genes (DEGs) and enriched pathways. POAG patients exhibited significant RNFL thinning, which correlated with both visual field loss and cognitive impairments, particularly in terms of visual memory and executive function. Transcriptomic profiling revealed a distinct gene expression signature in POAG, including upregulation of TTBK1 and CCN2 (CTGF), genes associated with tau phosphorylation and extracellular matrix remodeling. Functional enrichment analysis indicated the involvement of neurodegenerative pathways, such as glutamate signaling, calcium signaling, and cell adhesion. Our findings support the reclassification of glaucoma as a neurodegenerative disease with both ocular and cognitive manifestations. Furthermore, biomarkers such as TTBK1 and CCN2 may serve as potential targets for early detection and neuroprotective therapy.

Glaucoma is a common cause of visual loss and irreversible blindness, affecting visual and life quality. Various mechanisms are involved in retinal ganglion cell (RGC) apoptosis and functional and structural loss in the visual system. The prevalence of glaucoma has increased in several countries. However, its early diagnosis has contributed to prompt attention. Molecular and cellular biological mechanisms are important for understanding the pathological process of glaucoma and new therapies. Thus, this review discusses the factors involved in glaucoma, from basic science to cellular and molecular events (e.g., mitochondrial dysfunction, endoplasmic reticulum stress, glutamate excitotoxicity, the cholinergic system, and genetic and epigenetic factors), which in recent years have been included in the development of new therapies, management, and diagnosis of this disease.

The coronavirus family is a group of zoonotic viruses with some recognized reservoirs particularly some bats. A novel coronavirus emerged in the province of Wuhan (China) in December of 2019.The number of infected patient with serious respiratory infection quickly spread around the world to become a global pandemic. The clinical presentation and viral pathogenesis of the coronavirus disease named COVID-19 indicated that the virus is transmitted from person to person through infected droplets entering the respiratory mucosa. Close contact with infected individuals particularly in crowded environments has characterized the rapid spread of the infection.

The ongoing outbreak of COVID-19 challenges health systems and epidemiological responses of all countries worldwide. Although mitigation measures have been globally considered, the spatial heterogeneity of its effectiveness is evident, underscoring global health inequalities. Using Bayesian-based Markov chain Monte Carlo simulations, we evidenced that factors contributing to poverty are also risk factors for COVID-19 case-fatality, and unexpectedly, their impact on the case-fatality risk is comparable to that produced by health factors. Additionally, we confirm that both case-fatality risk and multidimensional poverty index have a heterogeneous spatial distribution, where the lastest consists of health, educational, dwelling, and employment dimensions. Spatio-temporal analysis reveals that the spatial heterogeneity in case-fatalities is associated with the percentage contribution of the health (RR 1.89 95%CI=1.43-2.48) and dwelling (RR 2.01 95%CI=1.37-2.63) dimensions to the multidimensional poverty, but also with the educational (RR 1.21 95%CI=1.03-1.49), and employment (RR 1.23 95%CI=1.02-1.47) dimensions. This spatial correlation indicates that the case-fatality risk increase by 189% and 201% in regions with a higher contribution of the health dimension (i.e., lack of health insurance and self-reporting) and dwelling dimension (i.e., lack of access to safe water, inadequate disposal of human feces, poor housing construction, and critical overcrowding), respectively. Furthermore, although a temporal decrease is evident, the relative risk of dying by COVID-19 in Colombia is still 200% higher than the established case-fatality risk based on the COVID-19 dynamics in Italy and China. These findings assist policy-makers in the spatial and temporal planning of strategies focused on mitigating the case-fatality risk in most vulnerable communities and preparing for future pandemics by progressively reducing the factors that generate health inequality.