Mouse Models of Corneal Neovascularization in the MICRON Literature

About the MICRON Research Literature

These research pages organize published studies using MICRON imaging systems by animal species and the disease or condition investigated.

All publication counts and figures reflect the complete indexed research collection.

Explore related studies through the MICRON Research Hubs or search the complete publication collection in the reSEARCH portal.

Understanding Corneal Neovascularization

Corneal neovascularization is the abnormal growth of new blood vessels from the limbus into the normally avascular corneal stroma. A healthy cornea maintains its transparency and remains free of blood vessels through several natural anti-angiogenic mechanisms.

These protective mechanisms include soluble vascular endothelial growth factor receptor-1 (sVEGFR-1), which binds VEGF-A, along with thrombospondins, pigment epithelium-derived factor (PEDF), and endostatin. Disruption of these mechanisms can lead to pathological corneal angiogenesis.

Common causes of corneal neovascularization include:

• Infection and corneal inflammation
• Hypoxia
• Chemical or thermal injury
• Surgical trauma, including corneal sutures
• Damage to the limbal barrier

New blood vessel growth may also be accompanied by lymphangiogenesis. Together, these changes can reduce corneal transparency, compromise ocular immune privilege, and increase the risk of corneal transplant rejection.

Corneal Neovascularization in Experimental Research

The cornea provides a useful experimental model for studying angiogenesis, inflammation, vascular growth, and anti-angiogenic therapies.

Because the normal cornea is transparent and avascular, researchers can induce neovascularization at a defined location and time, then monitor the development and regression of new vessels in the living eye.

Common experimental approaches include corneal sutures, stromal micropockets, implanted pellets, and injury-induced models. These methods allow researchers to investigate disease mechanisms and evaluate the effects of pro-angiogenic or anti-angiogenic compounds.

Animal models of corneal neovascularization generally serve two purposes:

• Disease modeling: Investigating the onset, progression, and treatment of corneal neovascularization.
• Angiogenesis assessment: Measuring vascular responses to experimental compounds, including therapies intended for other tissues.

Non-invasive, longitudinal imaging makes it possible to measure vessel growth, vascularized area, and treatment response over time, reducing the need for repeated tissue collection.

However, animal models do not fully reproduce human clinical outcomes. Visual impairment, long-term corneal graft survival, and chronic disease progression require clinical evaluation. Anatomical differences between rodent and human corneas, including corneal thickness and the distance from the limbus to the visual axis, must also be considered when interpreting vessel growth and regression.

Mouse Models of Corneal Neovascularization

Mice are the most frequently used species in this collection of corneal neovascularization studies.

Mouse models offer several advantages, including established experimental protocols, relatively low costs, short generation times, and extensive genetic resources.

Transgenic and knockout mouse models allow researchers to investigate the contribution of specific genes and signaling pathways to corneal angiogenesis. However, genetic modifications may also introduce developmental compensation or effects on multiple biological pathways, which should be considered when interpreting results.

Published MICRON Research: Corneal Neovascularization in Mice

This page lists 21 papers from the MICRON literature, published 2015 to 2026, that study corneal neovascularization in mice.

Of these publications:

• 20 studies used mice as the primary corneal neovascularization disease model.
• 1 study used healthy animals to assess pharmacokinetics, drug delivery, or tolerability.

Scope of the literature collection: Publication counts reflect studies identified and indexed in the MICRON research corpus. This collection is not intended to represent an exhaustive review of all published corneal neovascularization research.

Which imaging and experimental techniques are used in these studies?

Technique counts are paper-level co-occurrences and do not necessarily indicate that a technique was applied to the focal species or focal disease model.

Capabilities and Limitations of Imaging Techniques

A summary of what each imaging technique listed above can measure, the information it provides, and its limitations in research applications.

Optical Coherence Tomography

Optical coherence tomography provides high-resolution, cross-sectional images of ocular tissues in the living eye, allowing researchers to visualize structures at different depths. OCT is particularly useful for measuring tissue thickness, identifying structural abnormalities, and assessing the location and extent of tissue changes.

As a non-invasive imaging technique, OCT enables repeated measurements in the same eye over time, supporting longitudinal studies of disease progression and treatment response. Although OCT provides detailed structural information, it does not directly measure cellular activity or visual function. Tissue that appears structurally normal may still have functional abnormalities, making OCT a valuable companion to functional assessments such as electroretinography (ERG).

Topical Ophthalmic Drug Delivery

A compound applied as drops to the ocular surface. It is non-invasive and repeatable, so it supports frequent dosing without a procedure for each dose. What the route has to establish depends on the target: for an ocular-surface target, residence time and penetration into the surface tissue are the main barriers; for an intraocular anterior-segment target, the compound must cross ocular-surface and corneal or conjunctival barriers and reach an intraocular concentration sufficient for the experiment; for a posterior-segment target, additional ocular barriers separate the surface from the target and posterior-segment exposure is harder to establish.

Fundus Fluorescein Angiography

Fundus fluorescein angiography uses an injected fluorescent dye to visualize blood flow through the retinal and choroidal circulation. Sequential images show how vessels fill, identify areas of reduced or absent perfusion, and reveal dye leakage associated with vascular abnormalities.

This technique is particularly useful for evaluating vascular perfusion, blood-retinal barrier integrity, and abnormal vessel growth. Fluorescein angiography primarily shows dye distribution rather than the surrounding retinal tissue. It provides a two-dimensional (en face) view in which vessels at different depths may overlap. Cross-sectional and cellular structural details require other imaging methods, such as optical coherence tomography (OCT) or optical coherence tomography angiography (OCT-A). Vascular abnormalities that do not affect dye filling or produce leakage may also remain undetected.

Intravitreal Injection / Delivery

Injection into the vitreous places a substance directly into the vitreous at a known administered dose and chosen time, reducing but not eliminating systemic exposure. The injectate may be a therapeutic compound, cell preparation or viral vector, or an agent used to create the model, such as a toxin, vasoactive or excitotoxic compound, or infectious inoculum. The route bypasses surface-delivery barriers and provides direct access to the vitreous and posterior segment, but the concentration reached in a particular ocular tissue depends on distribution and clearance and is not fixed by the injected dose alone. It is invasive and discrete: each repeat dose or challenge requires another injection, and vehicle- or sham-injected controls can help separate effects of the injectate from effects of the procedure.

Laser Photocoagulation Models

A laser lesion provokes a reproducible, quantifiable injury at a known time and place. Wavelength, power, duration, spot size, pulse mode, focus and lesion location together determine the injury produced, allowing laser exposure to be configured for different experimental endpoints. It is an induced injury, not the disease: it produces a lesion directly, bypassing the process that gives rise to comparable damage in patients.

Electroretinography

Records the retina's electrical response to light, giving component-sensitive information about outer- and inner-retinal function. It measures function directly, which no structural method does. Full-field ERG sums across the whole retina, so a small lesion can leave the trace unchanged; focal and multifocal variants trade signal amplitude for spatial resolution.

Ocular Blast Injury

Experimental ocular blast models expose the eye, or in some paradigms the head with ocular outcomes measured, to a controlled overpressure wave at a known time. Peak pressure, waveform and impulse, exposure number, orientation and interval help determine the loading delivered to the eye. A blast wave can injure multiple ocular compartments, including anterior structures, retina and optic nerve, although the pattern and severity depend on the exposure paradigm and the animal. Eye-directed paradigms that shield the head and body are used to isolate primary blast effects on the eye; head-directed or less-confined paradigms may also involve central nervous-system and other traumatic-brain-injury mechanisms and should not be treated as equivalent. Because the exposure is known, interventions can be tested against it and sham exposures can help distinguish effects of the pressure wave from handling or the experimental procedure. Apparatus design, waveform, positioning and shielding materially affect the delivered exposure, so nominal pressure values or exposure counts should not be assumed directly comparable across laboratories or equivalent to human blast exposure without physical characterization.

Ocular Implants / Sustained Release

A sustained-release system holds a compound in or on the eye and lets it out gradually, so exposure is maintained from one placement rather than from a series of doses. The class spans polymer and non-polymer solid depots, injectable and particulate carriers, and reservoir devices; the release period belongs to the platform and not to the route, and runs from days to years. What the approach is for is to separate the dosing interval from the procedure interval, holding exposure at the target for as long as the question runs, whether that is the few weeks of a short-lived model or the span of a lifelong disease, without an intervention for each dose. What it gives up is control after placement. The release profile has to be measured rather than assumed, altering or ending delivery may require a further procedure, biodegradable systems behave differently from removable ones, and the carrier sits in contact with ocular tissue, so how the eye tolerates it is part of the result and not a precondition of it.

Which MICRON systems and add-ons appear?

Which strains and genetic lines are used?

Which other species appear alongside?

What other conditions are recorded on the same papers?

Which MICRON configurations appear in this work?

Configurations recorded in these papers, and the techniques recorded alongside them.

The papers

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