Autophagy modulation in animal models of corneal diseases: a systematic review
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Autophagy modulation in animal models of corneal diseases: a systematic review Guadalupe Martínez‑Chacón1,2,3,4 · Francisco Javier Vela1 · José Luis Campos1 · Elena Abellán1 · Sokhna M. S. Yakhine‑Diop2,3,4 · Alberto Ballestín1 Received: 14 March 2020 / Accepted: 11 July 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Autophagy is an intracellular catabolic process implicated in the recycling and degradation of intracellular components. Few studies have defined its role in corneal pathologies. Animal models are essential for understanding autophagy regulation and identifying new treatments to modulate its effects. A systematic review (SR) was conducted of studies employing animal models for investigations of autophagy in corneal diseases. Studies were identified using a structured search strategy (TS = autophagy AND cornea*) in Web of Science, Scopus, and PubMed from inception to September 2019. In this study, 230 articles were collected, of which 28 were analyzed. Mouse models were used in 82% of the studies, while rat, rabbit, and newt models were used in the other 18%. The most studied corneal layer was the epithelium, followed by the endothelium and stroma. In 13 articles, genetically modified animal models were used to study Fuch endothelial corneal dystrophy (FECD), granular corneal dystrophy type 2 (GCD2), dry eye disease (DED), and corneal infection. In other 13 articles, animal models were experimentally induced to mimic DED, keratitis, inflammation, and surgical scenarios. Furthermore, in 50% of studies, modulators that activated or inhibited autophagy were also investigated. Protective effects of autophagy activators were demonstrated, including rapamycin for DED and keratitis, lithium for FECD, LYN-1604 for DED, cysteamine and miR-34c antagomir for damaged corneal epithelium. Three autophagy suppressors were also found to have therapeutic effects, such as aminoimidazole-4-carboxamide-riboside (AICAR) for corneal allogeneic transplantation, celecoxib and chloroquine for DED. Keywords Autophagy · Animal model · Corneal disease · PRISMA · Systematic review
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11010-020-03832-5) contains supplementary material, which is available to authorized users.
Abbreviations AICAR Aminoimidazole-4-carboxamide riboside AMD Age-related macular degeneration AMPK AMP-activated protein kinase
* Guadalupe Martínez‑Chacón [email protected]
1
Department of Microsurgery, Jesús Usón Minimally Invasive Surgery Centre, 10071 Cáceres, Spain
Francisco Javier Vela [email protected]
2
Department of Biochemistry and Molecular Biology and Genetics, Faculty of Nursing and Occupational Therapy, University of Extremadura, Avda de La Universidad S/N, 10003 Cáceres, Spain
3
Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED), 28049 Madrid, Spain
4
Instituto Universitario de Investigación Biosanitaria de Extremadura (INUBE), 10003 Cáce
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