Mouse Models of Diabetic Retinopathy 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 Diabetic Retinopathy

Diabetic retinopathy (DR) is a microvascular complication of diabetes associated with prolonged hyperglycemia. Over time, elevated blood glucose damages the retinal vasculature, leading to structural and functional changes that can impair vision.

Common features of diabetic retinopathy include:

• Loss of retinal capillary pericytes
• Formation of microaneurysms
• Breakdown of the blood-retinal barrier and increased vascular leakage
• Capillary non-perfusion and retinal ischemia
• Pathological retinal neovascularization in advanced disease

Diabetic macular edema (DME) and complications of proliferative diabetic retinopathy (PDR) are major causes of vision loss in affected patients.

In addition to vascular damage, diabetic retinopathy is associated with retinal neurodegeneration and glial dysfunction. These changes may occur before clinically detectable vascular lesions or develop alongside them. Their precise relationship to the onset and progression of diabetic retinopathy remains an active area of research.

Diabetic Retinopathy in Experimental Research

Animal models of diabetic retinopathy allow researchers to investigate the effects of hyperglycemia on retinal structure, vascular integrity, inflammation, and visual function.

Diabetes can be induced experimentally through chemical destruction of pancreatic insulin-producing beta cells or through genetic alterations affecting insulin production or metabolic regulation, including leptin signaling.

These models reproduce several features of early diabetic retinal disease, including:

• Blood-retinal barrier dysfunction and vascular leakage
• Retinal capillary cell loss
• Inflammatory and metabolic changes
• Inner retinal thinning and neurodegeneration
• Altered electroretinogram (ERG) responses, including reduced amplitudes or delayed response times

Longitudinal retinal imaging and functional testing allow these changes to be monitored in the same animal over time, supporting investigations of disease progression and treatment response.

However, important anatomical and biological differences limit direct translation to human diabetic retinopathy.

Mice, rats, and rabbits lack a macula and therefore cannot reproduce diabetic macular edema in its human anatomical location. Retinal thickening and vascular leakage can still be investigated, but measurements are obtained outside macular anatomy.

Diabetic rodents also generally do not develop spontaneous proliferative diabetic retinopathy within their lifespan. Consequently, experimentally induced preretinal neovascularization should not be interpreted as the natural progression of diabetic retinopathy without additional supporting evidence.

Rabbits present another limitation because their retinal blood vessels are largely confined to the medullary rays, leaving much of the retina avascular. This vascular arrangement limits their suitability for studying diffuse retinal capillary disease.

Mouse Models of Diabetic Retinopathy

Mice are the most frequently used species in this literature collection investigating diabetic retinopathy.

Mouse models offer several advantages, including established experimental protocols, relatively low costs, short generation times, extensive background data, and access to genetically modified strains.

Common approaches include chemically induced diabetes and genetic models affecting insulin production, glucose metabolism, or leptin signaling.

Transgenic and knockout mouse models also allow researchers to investigate specific molecular pathways involved in retinal vascular injury, inflammation, and neurodegeneration.

However, genetic modifications may produce developmental compensation or affect multiple physiological pathways. These potential effects must be considered when interpreting experimental findings.

Mouse models are particularly valuable for investigating early diabetic retinal changes and evaluating experimental therapies, although they do not fully reproduce the advanced vascular complications observed in human proliferative diabetic retinopathy.

Published MICRON Research: Diabetic Retinopathy in Mice

This page lists 94 papers from the MICRON literature, published 2013 to 2026, that study diabetic retinopathy in mice.

Of these publications:

• 93 studies used mice as the primary diabetic retinopathy 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 diabetic retinopathy 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.

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.

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).

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.

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.

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.

AAV-Mediated Ocular Gene Delivery

An adeno-associated viral vector delivers genetic material to ocular cells, and a single administration can support long-lived transgene expression. That persistence is useful for gene augmentation and sustained therapeutic-protein expression; AAV can also deliver gene-silencing or genome-editing cargo, where long-lived expression of the editing machinery may be unnecessary or undesirable. Capsid and route of delivery jointly determine which cells are reached, so different delivery routes and vector designs give different distributions.

CRISPR-Based Ocular Gene Editing

Uses a programmable genome-editing system to alter DNA at an endogenous locus rather than adding a separate replacement copy. Depending on the editor and design, it can disrupt, correct or install a sequence, either therapeutically or to create an experimental model. Once a genomic sequence change is established, the edit itself cannot be withdrawn like a dose; where the edit is present from conception, the resulting phenotype also reflects its effects throughout development. Off-target sequence changes are a separate question that structural imaging does not establish.

Optokinetic / Optomotor Response

Measures a reflexive head or eye movement tracking a moving pattern, giving a rapid, training-free behavioral estimate of spatial vision and contrast sensitivity in an animal that cannot report them. It is driven largely by reflex circuitry and reports on the visual pathway as a whole, so a deficit it detects still has to be localized by a structural or electrophysiological method, or separated from cortical processing by an operant task.

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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