Aims and Scope
International Journal of Glaucoma (IJG) publishes mechanistic research on glaucoma pathophysiology, focusing on molecular pathways, cellular mechanisms, disease biomarkers, and pathogenic processes underlying glaucomatous optic neuropathy and intraocular pressure dysregulation.
Core Research Domains
Molecular Pathophysiology of Glaucoma
Mechanistic investigation of cellular and molecular processes driving glaucomatous neurodegeneration and trabecular meshwork dysfunction.
- Retinal ganglion cell death mechanisms (apoptosis, necroptosis, autophagy)
- Trabecular meshwork extracellular matrix remodeling pathways
- Mitochondrial dysfunction and oxidative stress in glaucoma
- Neuroinflammatory signaling cascades in optic nerve degeneration
- Aqueous humor outflow pathway molecular regulation
- Axonal transport disruption mechanisms in glaucomatous optic neuropathy
"ROCK pathway activation mediates trabecular meshwork contractility and extracellular matrix deposition in primary open-angle glaucoma: molecular mechanisms and biomarker validation"
Genetic & Epigenetic Mechanisms
Molecular genetics, gene expression regulation, and epigenetic modifications underlying glaucoma susceptibility and progression.
- MYOC, OPTN, TBK1 gene mutation pathophysiology
- Polygenic risk mechanisms in primary open-angle glaucoma
- DNA methylation patterns in trabecular meshwork cells
- MicroRNA regulation of glaucoma-associated genes
- Histone modification in retinal ganglion cell survival pathways
- Gene-environment interaction mechanisms in glaucoma pathogenesis
"Epigenetic silencing of neuroprotective genes through CpG island hypermethylation in glaucomatous retinal ganglion cells: mechanistic pathway analysis"
Intraocular Pressure Regulation Mechanisms
Cellular and molecular mechanisms controlling aqueous humor dynamics, outflow resistance, and pressure-induced tissue damage.
- Schlemm's canal endothelial cell mechanotransduction pathways
- Ciliary body epithelial aqueous humor secretion mechanisms
- Conventional and unconventional outflow pathway molecular regulation
- Pressure-induced mechanosensitive ion channel activation
- Extracellular matrix stiffness effects on trabecular meshwork function
- Circadian rhythm molecular control of intraocular pressure
"Piezo1 mechanosensitive channel activation in trabecular meshwork cells: molecular mechanisms linking mechanical stress to outflow resistance in glaucoma"
Biomarker Discovery & Validation
Identification and mechanistic characterization of molecular, cellular, and biochemical biomarkers for glaucoma pathophysiology.
- Aqueous humor proteomic and metabolomic biomarker profiling
- Retinal ganglion cell-specific molecular markers of neurodegeneration
- Circulating microRNA signatures in glaucoma progression
- Tear film biomarkers reflecting ocular surface inflammation
- Optic nerve head tissue biomarkers of structural damage
- Genetic biomarkers for disease susceptibility and progression risk
"Aqueous humor metabolomic profiling reveals dysregulated amino acid metabolism as early biomarker of glaucomatous neurodegeneration: pathway analysis and validation"
Secondary Focus Areas
Disease Models & Experimental Systems
Development and characterization of in vitro, ex vivo, and in vivo models for mechanistic glaucoma research. Includes cellular models, organoid systems, and animal models with focus on pathophysiological relevance and translational potential.
Neurodegeneration Mechanisms
Molecular pathways shared between glaucomatous optic neuropathy and other neurodegenerative diseases. Includes excitotoxicity, protein misfolding, neuroinflammation, and synaptic dysfunction mechanisms with cross-disease implications.
Vascular & Hemodynamic Mechanisms
Molecular regulation of ocular blood flow, endothelial dysfunction, and vascular dysregulation in glaucoma pathogenesis. Includes hypoxia-inducible pathways, endothelial nitric oxide signaling, and autoregulation mechanisms.
Immune & Inflammatory Pathways
Innate and adaptive immune mechanisms in glaucoma, including complement activation, microglial responses, T-cell mediated neurodegeneration, and autoimmune components of disease progression.
Glial Cell Pathophysiology
Molecular mechanisms of astrocyte and microglial activation, reactive gliosis, and glial-neuronal interactions in glaucomatous neurodegeneration. Includes glial inflammatory responses and neuroprotective signaling pathways.
Methodological Innovations
Novel techniques for studying glaucoma pathophysiology, including advanced imaging modalities for cellular mechanisms, omics technologies, single-cell analysis, and computational modeling of disease processes.
Emerging Research Frontiers
Single-Cell Molecular Profiling
Single-cell RNA sequencing, proteomics, and spatial transcriptomics revealing cellular heterogeneity and cell-type-specific mechanisms in glaucomatous tissues. Note: Requires additional editorial review for mechanistic depth.
Mechanistic Drug Target Discovery
Identification and validation of molecular targets for neuroprotection and disease modification. Focus on pathway-based target discovery, not clinical drug development or therapeutic outcomes.
Systems Biology Approaches
Network analysis, pathway modeling, and multi-omics integration to understand complex molecular interactions in glaucoma pathogenesis. Computational models must be experimentally validated.
Mechanistic Aging Research
Molecular mechanisms linking cellular senescence, age-related mitochondrial dysfunction, and oxidative damage to glaucoma susceptibility. Focus on mechanistic pathways, not epidemiological associations.
Explicitly Out of Scope
Clinical Treatment & Surgical Techniques
Rationale: Clinical management, surgical procedures (trabeculectomy, tube shunts, MIGS), laser treatments, and therapeutic protocols are outside our pathophysiology focus. These belong in clinical ophthalmology journals.
Patient Outcomes & Quality of Life
Rationale: Studies on visual function outcomes, patient-reported measures, healthcare accessibility, or socioeconomic impacts lack mechanistic focus. These are appropriate for public health or clinical journals.
Diagnostic Technology & Imaging Devices
Rationale: Clinical validation of OCT devices, visual field testing protocols, or diagnostic algorithms without mechanistic investigation of disease processes are not within scope. Device performance studies belong elsewhere.
Epidemiological Studies Without Mechanism
Rationale: Pure prevalence studies, risk factor associations, or population trends without molecular/cellular mechanistic investigation do not fit our pathophysiology mandate. Epidemiology journals are more appropriate.
Non-Glaucoma Ocular Conditions
Rationale: Myopia, diabetic retinopathy, aneurysm, myasthenia gravis, and other non-glaucomatous conditions are outside journal scope unless directly investigating shared molecular mechanisms with glaucoma pathophysiology.
Article Types & Editorial Priorities
Mechanistic Research & Methods
Brief Communications & Data
Limited Acceptance
Editorial Standards & Requirements
Reporting Guidelines
- ARRIVE 2.0 for animal studies
- MIQE for qPCR experiments
- PRISMA for systematic reviews
- STROBE for observational studies (if mechanistic)
- Transparent reporting of methods and statistics
Data & Reproducibility
- Raw data deposition in public repositories
- Complete reagent and antibody validation
- Statistical analysis code availability
- Biological replicates clearly stated
- Negative controls and validation experiments
Ethics & Integrity
- IACUC approval for animal research
- IRB approval for human tissue studies
- Informed consent documentation
- Conflict of interest disclosure
- Adherence to COPE guidelines
Preprint & Prior Publication
- Preprints welcomed (bioRxiv, medRxiv)
- Must disclose preprint DOI at submission
- Conference abstracts acceptable
- No prior publication in peer-reviewed journals
- Preprint servers do not constitute prior publication
Editorial Performance Metrics
Questions About Scope Fit?
If your research focuses on molecular mechanisms, cellular pathways, or disease biomarkers in glaucoma pathophysiology, we encourage submission. For scope inquiries or pre-submission questions, contact our editorial team.
