Dry eye disease (DED), which is a prevalent disease that still lacks successful treatment options, remains a major challenge in ophthalmology. Multiple animal models of DED have been used to decipher its pathophysiology and to develop novel treatments. These models use mice, rats, rabbits, cats, dogs and non-human primates. Each model assesses aspects of DED by focusing on elements of the lacrimal functional unit, which controls the homeostasis of the tear film. The present review outlines representative DED animal models and assesses their contribution to the study of DED. Murine models are the most extensively used, followed by rabbit models; the latter offer the advantage of larger eyes, a favorable biochemical profile for drug studies, experimental ease and relatively low cost, contrasting with non-human primates, which, although closer to humans, are not as accessible and are expensive. No comprehensive 'ideal' animal model encompassing all aspects of human DED exists nor is it feasible. Investigators often choose an animal model based on their experimental needs and the following four features of a given model: The size of the eye, its biochemical composition, the available research reagents and cost. As research efforts in DED expand, more refined animal models are needed to supplement the enormous contribution made to date by existing models.
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http://dx.doi.org/10.3892/etm.2021.10830 | DOI Listing |
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Department of Hematology and Medical Oncology, Emory University, 201 Dowman Dr, Atlanta, GA, 30322, USA.
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Biomark Res
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View Article and Find Full Text PDFBMC Microbiol
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Department of Laboratory Medicine, the Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, P.R. China.
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Hum Cell
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Department of Nephrology, Zhong Da Hospital, Gulou District, No. 87, Dingjiaqiao, Zhongyangmen Street, Nanjing, 210009, Jiangsu, China.
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View Article and Find Full Text PDFIn Vitro Cell Dev Biol Anim
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Department of Biology, Wilfrid Laurier University, 75 University Avenue West, Waterloo, ON, N2L 3C5, Canada.
Long dsRNA induces the expression of type I interferons (IFNs) and IFN-stimulated genes (ISGs) to establish an antiviral state. When induced prophylactically, this antiviral state can reduce the severity and mortality of viral infections. One of the limiting factors in delivering dsRNA in animal models is the lack of an effective carrier that protects the dsRNA from degradation in the extracellular space.
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