International Journal of Glaucoma

International Journal of Glaucoma

International Journal of Glaucoma – About

Open Access & Peer-Reviewed

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International Journal of Glaucoma

Advancing the mechanistic understanding of glaucomatous neurodegeneration through peer-reviewed pathophysiology research

Exploring Molecular Mechanisms of Glaucomatous Disease

The International Journal of Glaucoma (IJG) is a peer-reviewed, open access publication dedicated to advancing our understanding of the cellular and molecular pathophysiology underlying glaucoma. Published by Open Access Pub, IJG provides a specialized platform for researchers investigating disease mechanisms, biomarker discovery, and the fundamental biological processes that drive optic nerve degeneration and retinal ganglion cell death.

Our mission is to illuminate how glaucoma works at the molecular level—from genetic susceptibility factors and intraocular pressure dynamics to mitochondrial dysfunction, neuroinflammation, axonal transport failure, and excitotoxicity. By focusing on mechanistic understanding rather than clinical therapeutics, IJG fills a critical niche for basic science researchers, molecular biologists, and translational investigators seeking to uncover the root causes of glaucomatous neuropathy.

Our Pathophysiology-Focused Scope

IJG concentrates exclusively on the mechanistic foundations of glaucoma—not clinical diagnosis, surgical techniques, or patient management protocols. We publish research that reveals disease pathways, biomarker signatures, cellular stress responses, and molecular targets with the potential to inform future therapeutic development.

Our editorial philosophy prioritizes manuscripts that advance mechanistic insight through experimental models, molecular analyses, genetic studies, and systems biology approaches. Whether investigating aqueous humor dynamics, trabecular meshwork pathology, oxidative stress cascades, or neuronal apoptosis mechanisms, IJG serves as the premier venue for glaucoma pathophysiology scholarship.

Within Scope: Mechanistic Research

  • Molecular pathways of retinal ganglion cell death
  • Genetic and epigenetic risk factors
  • Cellular stress responses and mitochondrial dysfunction
  • Biomarker discovery and validation studies
  • Disease models (in vitro, animal, computational)
  • Neuroinflammation and immune mechanisms
  • Extracellular matrix remodeling in glaucoma
  • Molecular mechanisms of intraocular pressure regulation

Outside Scope: Clinical Practice

  • Surgical technique descriptions or case series
  • Clinical diagnostic protocols or screening guidelines
  • Patient management strategies or treatment algorithms
  • Comparative effectiveness of therapies
  • Quality of life or health economic analyses
  • Clinical trial outcomes without mechanistic focus
  • Device evaluations or procedural innovations
Research Pillars

Mechanistic Areas of Focus

  • Molecular Genetics & Genomics: Gene variants, GWAS findings, transcriptomic profiling, and hereditary glaucoma mechanisms
  • Cellular Pathophysiology: Trabecular meshwork dysfunction, retinal ganglion cell vulnerability, glial activation, and neuronal death pathways
  • Biomechanics & Intraocular Pressure: Aqueous humor dynamics, scleral stiffness, lamina cribrosa deformation, and pressure-induced stress
  • Oxidative Stress & Mitochondrial Function: Reactive oxygen species, mitochondrial damage, energy metabolism, and antioxidant defenses
  • Neuroinflammation & Immunity: Microglia activation, cytokine signaling, complement pathways, and autoimmune contributions
  • Vascular & Perfusion Mechanisms: Ocular blood flow regulation, endothelial dysfunction, and ischemic injury pathways
  • Protein Homeostasis & Degradation: Protein aggregation, autophagy, endoplasmic reticulum stress, and protein quality control
  • Biomarker Discovery: Proteomic, metabolomic, and imaging biomarkers for disease staging or progression prediction
Types of Mechanistic Submissions

IJG welcomes diverse research formats that advance mechanistic understanding of glaucoma pathophysiology:

Original Research Articles

Reports of experimental findings elucidating molecular mechanisms, disease pathways, or cellular responses in glaucoma models.

Mechanistic Reviews

Comprehensive syntheses of molecular mechanisms, pathway analyses, or emerging concepts in glaucoma pathophysiology.

Biomarker Studies

Discovery and validation research identifying molecular, proteomic, or imaging signatures associated with disease mechanisms.

Model Development

Characterization of in vitro, animal, or computational models that recapitulate glaucomatous pathology for mechanistic investigation.

Molecular Case Reports

Rare genetic variants or atypical molecular phenotypes offering mechanistic insights into disease heterogeneity.

Short Communications

Concise reports of significant mechanistic findings, methodological innovations, or preliminary observations warranting rapid dissemination.

Methodological Rigor: All submissions undergo rigorous peer review by experts in molecular biology, neuroscience, genetics, and glaucoma pathophysiology. Manuscripts must demonstrate experimental reproducibility, appropriate controls, statistical validity, and clear mechanistic interpretation. We adhere to COPE guidelines and require compliance with institutional review standards for human samples and animal research.

Why Publish Mechanistic Research in IJG?
1

Specialized Focus

Dedicated platform for pathophysiology research without scope dilution from clinical or surgical content.

2

Expert Review

Manuscripts evaluated by molecular biologists and mechanistic specialists in glaucoma research.

3

Rapid Dissemination

Accelerated peer review and publication timelines to advance scientific discourse quickly.

4

Open Access

Immediate, unrestricted access ensures maximum visibility for mechanistic discoveries globally.

Mechanisms We Investigate

Retinal Ganglion Cell Death

Apoptosis pathways, axonal degeneration, neurotrophic factor deprivation, and mechanisms of selective neuronal vulnerability.

Intraocular Pressure Dysregulation

Trabecular meshwork stiffness, aqueous outflow resistance, extracellular matrix changes, and pressure-sensing mechanisms.

Oxidative Damage

Reactive oxygen species generation, mitochondrial dysfunction, lipid peroxidation, and antioxidant system failure.

Neuroinflammatory Cascades

Microglial activation, cytokine networks, complement activation, and immune cell infiltration in optic nerve head.

Genetic Susceptibility

MYOC, OPTN, TBK1 mutations; polygenic risk scores; gene-environment interactions; and epigenetic modifications.

Biomechanical Stress

Scleral biomechanics, lamina cribrosa deformation, mechanical strain on axons, and tissue remodeling responses.

Editorial Excellence & Integrity

The IJG editorial board comprises internationally recognized experts in glaucoma pathophysiology, molecular neurobiology, genetics, and disease modeling. Our editors ensure manuscripts meet rigorous standards for experimental design, data interpretation, and mechanistic clarity.

We are committed to transparent peer review, ethical publishing practices, and reproducible research. Authors must provide detailed methods, data availability statements, and comply with institutional ethics approvals for all human and animal studies.

Submission Process: Researchers are encouraged to submit manuscripts that align with our mechanistic focus. Detailed author guidelines specify formatting requirements, reporting standards (e.g., ARRIVE for animal studies), and data sharing expectations. Submissions undergo rigorous peer review with constructive feedback to strengthen mechanistic interpretation and experimental rigor.

Advance Glaucoma Pathophysiology Research

Join the global community of scientists unraveling the molecular mysteries of glaucoma. Share your mechanistic discoveries, biomarker studies, or disease models with IJG to accelerate understanding of this complex neurodegenerative disease.

Contact the Editorial Office: For inquiries regarding scope alignment, special thematic collections, or mechanistic research suitable for IJG, contact [email protected]. We welcome dialogue with investigators exploring novel molecular mechanisms of glaucomatous neurodegeneration.