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Table 1. Laboratory-based studies demonstrating the engagement of autophagy in age-related eye diseasesAge-related eye diseasesSourceYearMethodResultsDry eye diseaseZoukhri, D. et al.PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5ab3VraHJpPC9BdXRob3I+PFllYXI+MjAwODwvWWVhcj48
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ADDIN EN.CITE.DATA [1]2008In vivoLacrimal gland acinar cells are lost through apoptosis and autophagy is induced by inflammation.Wang, N. et al.PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5XYW5nPC9BdXRob3I+PFllYXI+MjAxMzwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [2]2013In vitroLacritin can stimulate autophagy to restore homeostasis and plays a protective role in the dry eye.Tony, L. et al. ADDIN EN.CITE <EndNote><Cite><Author>Lin</Author><Year>2017</Year><RecNum>268</RecNum><DisplayText>[3]</DisplayText><record><rec-number>268</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1532166176">268</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Lin, T.</author><author>Filek, R.</author><author>Wang, J. M.</author><author>Wu, C. H.</author><author>Liu, H.</author><author>Hutnik, C. M.</author></authors></contributors><auth-address>Department of Ophthalmology, Western University.
Ivey Eye Institute, St Joseph's Health Care, St Joseph's Hospital.
Department of Pathology and Laboratory Medicine.
Department of Biology, Western University, London, ON, Canada.</auth-address><titles><title>Impression cytology implicates cell autophagy in aqueous deficiency dry eye</title><secondary-title>Clin Ophthalmol</secondary-title><alt-title>Clinical ophthalmology (Auckland, N.Z.)</alt-title></titles><pages>773-779</pages><volume>11</volume><edition>2017/06/13</edition><dates><year>2017</year></dates><isbn>1177-5467 (Print)
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ADDIN EN.CITE.DATA [5]2013In vivo/vitroDram1 is associated with increased autophagy. Overexpression of this gene in mouse and human FECD endothelial cells suggests a role for altered autophagy in FECD.Kim, E. C. et al.PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5LaW08L0F1dGhvcj48WWVhcj4yMDEzPC9ZZWFyPjxSZWNO
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ADDIN EN.CITE.DATA [6]2013In vivo/vitroIncreased autophagy in lithium treated endothelium in a mouse model of FECD reveals autophagy may contribute to increased endothelial cell survival.Benischke, A. S. et al. ADDIN EN.CITE <EndNote><Cite><Author>Benischke</Author><Year>2017</Year><RecNum>571</RecNum><DisplayText>[7]</DisplayText><record><rec-number>571</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1538891816">571</key><key app="ENWeb" db-id="">0</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Benischke, A. S.</author><author>Vasanth, S.</author><author>Miyai, T.</author><author>Katikireddy, K. R.</author><author>White, T.</author><author>Chen, Y.</author><author>Halilovic, A.</author><author>Price, M.</author><author>Price, F., Jr.</author><author>Liton, P. B.</author><author>Jurkunas, U. V.</author></authors></contributors><auth-address>Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA.
Price Vision Group, Indianapolis, IN, USA.
Department of Ophthalmology, Duke University, Durham, NC, USA.
Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. ula_jurkunas@meei.harvard.edu.</auth-address><titles><title>Activation of mitophagy leads to decline in Mfn2 and loss of mitochondrial mass in Fuchs endothelial corneal dystrophy</title><secondary-title>Sci Rep</secondary-title><alt-title>Scientific reports</alt-title></titles><pages>6656</pages><volume>7</volume><number>1</number><dates><year>2017</year><pub-dates><date>Jul 27</date></pub-dates></dates><isbn>2045-2322 (Electronic)
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ADDIN EN.CITE.DATA [8]2014In vitroAutophagy is activated in TM cells when subjected to biaxial static stretch (20% elongation), as well as in high-pressure perfused eyes (30 mm Hg).Porter, K. et al. ADDIN EN.CITE <EndNote><Cite><Author>Porter</Author><Year>2015</Year><RecNum>327</RecNum><DisplayText>[9]</DisplayText><record><rec-number>327</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1532231188">327</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Porter, K.</author><author>Hirt, J.</author><author>Stamer, W. D.</author><author>Liton, P. B.</author></authors></contributors><auth-address>Duke University, Department of Ophthalmology, Durham, NC, USA.
Duke University, Department of Ophthalmology, Durham, NC, USA. Electronic address: paloma.liton@dm.duke.edu.</auth-address><titles><title>Autophagic dysregulation in glaucomatous trabecular meshwork cells</title><secondary-title>Biochim Biophys Acta</secondary-title><alt-title>Biochimica et biophysica acta</alt-title></titles><pages>379-85</pages><volume>1852</volume><number>3</number><edition>2014/12/09</edition><keywords><keyword>*Autophagy</keyword><keyword>Cells, Cultured</keyword><keyword>Eye Proteins/*metabolism</keyword><keyword>Glaucoma, Open-Angle/*metabolism/pathology</keyword><keyword>Humans</keyword><keyword>Intraocular Pressure</keyword><keyword>*Oxidative Stress</keyword><keyword>*Proteolysis</keyword><keyword>Trabecular Meshwork/*metabolism/pathology</keyword></keywords><dates><year>2015</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>0006-3002 (Print)
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ADDIN EN.CITE.DATA [10]2015In vitroPhosphorylation of Ser177 serves as a crucial role in M98K-OPTN-induced autophagosome formation, autophagy flux and retinal cell death.Table 1. ContinuedAge-related eye diseasesSourceYearMethodResultsGlaucomaShim, M. S. et al. ADDIN EN.CITE <EndNote><Cite><Author>Shim</Author><Year>2016</Year><RecNum>689</RecNum><DisplayText>[11]</DisplayText><record><rec-number>689</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1543410556">689</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Shim, M. S.</author><author>Takihara, Y.</author><author>Kim, K. Y.</author><author>Iwata, T.</author><author>Yue, B. Y.</author><author>Inatani, M.</author><author>Weinreb, R. N.</author><author>Perkins, G. A.</author><author>Ju, W. K.</author></authors></contributors><auth-address>Hamilton Glaucoma Center, Department of Ophthalmology, and Shiley Eye Institute, University of California San Diego, La Jolla, CA, USA.
Department of Ophthalmology, Faculty of Medical Science, University of Fukui, Fukui, Japan.
Center for Research in Biological Systems, National Center for Microscopy and Imaging Research and Department of Neuroscience, University of California San Diego, La Jolla, CA, USA.
Division of Molecular and Cellular Biology, National Institute of Sensory Organs, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Department of Ophthalmology and Visual Sciences, College of Medicine, University of Illinois at Chicago, IL USA.</auth-address><titles><title>Mitochondrial pathogenic mechanism and degradation in optineurin E50K mutation-mediated retinal ganglion cell degeneration</title><secondary-title>Sci Rep</secondary-title><alt-title>Scientific reports</alt-title></titles><pages>33830</pages><volume>6</volume><edition>2016/09/23</edition><dates><year>2016</year><pub-dates><date>Sep 22</date></pub-dates></dates><isbn>2045-2322</isbn><accession-num>27654856</accession-num><urls></urls><custom2>Pmc5031982</custom2><electronic-resource-num>10.1038/srep33830</electronic-resource-num><remote-database-provider>Nlm</remote-database-provider><language>eng</language></record></Cite></EndNote>[11]2016In vivo/vitroE50K expression induces mitochondrial fission-mediated mitochondrial degradation and mitophagy in the axons of the glial lamina of aged E50K(-tg) mice in vivo.CataractCostello, M. J. et al.PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Db3N0ZWxsbzwvQXV0aG9yPjxZZWFyPjIwMTM8L1llYXI+
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ADDIN EN.CITE.DATA [12]2013In vitroAutophagy and mitophagy can be observed in epithelia from older human donor lenses.Zhou, J. et al. ADDIN EN.CITE <EndNote><Cite><Author>Zhou</Author><Year>2016</Year><RecNum>391</RecNum><DisplayText>[13]</DisplayText><record><rec-number>391</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1532236989">391</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Zhou, J.</author><author>Yao, K.</author><author>Zhang, Y.</author><author>Chen, G.</author><author>Lai, K.</author><author>Yin, H.</author><author>Yu, Y.</author></authors></contributors><auth-address>Eye Center, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China; Department of Otolaryngology, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Eye Center, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Department of Public Health, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</auth-address><titles><title>Thioredoxin Binding Protein-2 Regulates Autophagy of Human Lens Epithelial Cells under Oxidative Stress via Inhibition of Akt Phosphorylation</title></titles><pages>4856431</pages><volume>2016</volume><dates><year>2016</year></dates><isbn>1942-0994</isbn><accession-num>27656263</accession-num><urls></urls><remote-database-provider>Nlm</remote-database-provider></record></Cite></EndNote>[13]2016In vitroAutophagic response of lens epithelial cells with increased LC3-II and p62 can be induced by oxidative stress in age-related cataract and Thioredoxin binding protein-2 (TBP-2) regulates this response.AMDSaadat, K. A. et al. ADDIN EN.CITE <EndNote><Cite><Author>Saadat</Author><Year>2014</Year><RecNum>328</RecNum><DisplayText>[14]</DisplayText><record><rec-number>328</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1532231188">328</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Saadat, K. A.</author><author>Murakami, Y.</author><author>Tan, X.</author><author>Nomura, Y.</author><author>Yasukawa, T.</author><author>Okada, E.</author><author>Ikeda, Y.</author><author>Yanagi, Y.</author></authors></contributors><auth-address>Department of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Department of Ophthalmology and Visual Science, Nagoya City University Graduate School of Medical Sciences, Aichi 467-8601, Japan.
Okada Eye Clinic, Kanagawa 234-0054, Japan.</auth-address><titles><title>Inhibition of autophagy induces retinal pigment epithelial cell damage by the lipofuscin fluorophore A2E</title><secondary-title>FEBS Open Bio</secondary-title><alt-title>FEBS open bio</alt-title></titles><pages>1007-14</pages><volume>4</volume><edition>2014/12/05</edition><dates><year>2014</year></dates><isbn>2211-5463 (Print)
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ADDIN EN.CITE.DATA [15]2015In vitroA2E induces autophagy and decreases cell viability in a concentration- and time-dependent manner. The augmentation of autophagy can reduce the adverse effects of A2E.Perusek, L. et al.PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QZXJ1c2VrPC9BdXRob3I+PFllYXI+MjAxNTwvWWVhcj48
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ADDIN EN.CITE.DATA [16]2015In vivo/vitroAtg7 deficiency doses not severely affect the health of RPE cells in mice and A2E accumulation is independent of Atg7-mediated autophagy in RPE cells.Baek, A. et al.PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5CYWVrPC9BdXRob3I+PFllYXI+MjAxNzwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [18]2017In vitroP62is up-regulated in RPE cells under H2O2-induced oxidative stress and can promots autophagic activity.Sheu, S. J. et al. ADDIN EN.CITE <EndNote><Cite><Author>Sheu</Author><Year>2019</Year><RecNum>786</RecNum><DisplayText>[19]</DisplayText><record><rec-number>786</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1564223072">786</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Sheu, S. J.</author><author>Chen, J. L.</author><author>Bee, Y. S.</author><author>Lin, S. H.</author><author>Shu, C. W.</author></authors></contributors><auth-address>Department of Ophthalmology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.
School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Department of Optometry, Shu-Zen Junior College of Medicine and Management, Kaohsiung, Taiwan.
Yuh-Ing Junior College of Health Care and Management, Kaohsiung, Taiwan.
National Defense Medical Center, Taipei, Taiwan.
School of Medicine for International Students, I-Shou University, Kaohsiung, Taiwan.
Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan.</auth-address><titles><title>ERBB2-modulated ATG4B and autophagic cell death in human ARPE19 during oxidative stress</title><secondary-title>PLoS One</secondary-title><alt-title>PloS one</alt-title></titles><pages>e0213932</pages><volume>14</volume><number>3</number><edition>2019/03/15</edition><dates><year>2019</year></dates><isbn>1932-6203</isbn><accession-num>30870514</accession-num><urls><related-urls><url>;[19]2019In vitroErb-b2 receptor tyrosine-protein kinase 2 (ERBB2) can modulate ATG4B for autophagy induction and increased autophagy leads to autophagic cell death in oxidative stress-stimulated ARPE-19 cells.Table 1. ContinuedAge-related eye diseasesSourceYearMethodResultsDRPiano, I. et al. ADDIN EN.CITE <EndNote><Cite><Author>Piano</Author><Year>2016</Year><RecNum>418</RecNum><DisplayText>[20]</DisplayText><record><rec-number>418</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1532237331">418</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Piano, I.</author><author>Novelli, E.</author><author>Della Santina, L.</author><author>Strettoi, E.</author><author>Cervetto, L.</author><author>Gargini, C.</author></authors></contributors><auth-address>Department of Pharmacy, University of Pisa Pisa, Italy.
National Research Council (CNR), Neuroscience Institute Pisa, Italy.</auth-address><titles><title>Involvement of Autophagic Pathway in the Progression of Retinal Degeneration in a Mouse Model of Diabetes</title><secondary-title>Front Cell Neurosci</secondary-title><alt-title>Frontiers in cellular neuroscience</alt-title></titles><pages>42</pages><volume>10</volume><edition>2016/03/01</edition><dates><year>2016</year></dates><isbn>1662-5102 (Print)
1662-5102</isbn><accession-num>26924963</accession-num><urls><related-urls><url>;[20]2016In vivoInitial dysregulation of autophagy results in photoreceptor death in the early phase of DR.Jacqueline M. et al. ADDIN EN.CITE <EndNote><Cite><Author>Jacqueline M.Lopes de Faria</Author><Year>2016</Year><RecNum>654</RecNum><DisplayText>[21]</DisplayText><record><rec-number>654</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1540387596">654</key><key app="ENWeb" db-id="">0</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Jacqueline M.Lopes de Faria,</author><author> Diego A. Duarte,</author><author>Chiara Montemurro,</author><author>Alexandros Papadimitriou</author></authors></contributors><titles><title>Defective Autophagy in Diabetic Retinopathy</title></titles><dates><year>2016</year></dates><urls></urls><electronic-resource-num>10.1167/</electronic-resource-num></record></Cite></EndNote>[21]2016In vitroHigh glucose upregulates autophagy but p62/SQTSM1 cargo can be accumulated due to lysosomal dysfunction, resulting in massive VEGF release and rMCs death.Fu, D. et al.PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5GdTwvQXV0aG9yPjxZZWFyPjIwMTY8L1llYXI+PFJlY051
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ADDIN EN.CITE.DATA [22]2016In vitroAutophagy increases in retina under diabetic models. It has a dual role in DR.RAOOuimet, M. et al. ADDIN EN.CITE <EndNote><Cite><Author>Ouimet</Author><Year>2012</Year><RecNum>857</RecNum><DisplayText>[23]</DisplayText><record><rec-number>857</rec-number><foreign-keys><key app="EN" db-id="s2vx595dj5errtewferxtw9mz00e5xs9daee" timestamp="1566017079">857</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Ouimet, M.</author><author>Marcel, Y. L.</author></authors></contributors><auth-address>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, ON, K1Y4W7, Canada.</auth-address><titles><title>Regulation of lipid droplet cholesterol efflux from macrophage foam cells</title><secondary-title>Arterioscler Thromb Vasc Biol</secondary-title><alt-title>Arteriosclerosis, thrombosis, and vascular biology</alt-title></titles><pages>575-81</pages><volume>32</volume><number>3</number><edition>2011/12/31</edition><keywords><keyword>Animals</keyword><keyword>Atherosclerosis/*metabolism/pathology</keyword><keyword>Autophagy</keyword><keyword>Biological Transport</keyword><keyword>Cholesterol/*metabolism</keyword><keyword>Cholesterol Esters/metabolism</keyword><keyword>Foam Cells/*metabolism/pathology</keyword><keyword>Humans</keyword><keyword>Hydrolysis</keyword><keyword>Lipolysis</keyword><keyword>Sterol Esterase/metabolism</keyword></keywords><dates><year>2012</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>1079-5642</isbn><accession-num>22207731</accession-num><urls></urls><electronic-resource-num>10.1161/atvbaha.111.240705</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>[23]2012In vitroLipid loadingcan activate autophagy and cytoplasmic lipid droplets are delivered to lysosomes via autophagy.Razani, B. et al.PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5SYXphbmk8L0F1dGhvcj48WWVhcj4yMDEyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [24]2012In vivoDysfunction and deficiency of autophagy promotes atherosclerosis in part through inflammasome hyperactivation.Abbreviations. Type 2 granular corneal dystrophy (GCD2), Fuchs endothelial corneal dystrophy (FECD), Fuchs endothelial corneal dystrophy (FECD), trabecular meshwork (TM), Age-related macular degeneration (AMD), retinal pigment epithelial (RPE), diabetic retinopathy (DR), Retinal artery occlusion (RAO).References ADDIN EN.REFLIST [1] D. Zoukhri, A. Fix, J. Alroy and C. L. Kublin, "Mechanisms of murine lacrimal gland repair after experimentally induced inflammation," Invest Ophthalmol Vis Sci, vol. 49, no. 10, pp. 4399-4406, 2008.[2] N. Wang, K. Zimmerman, R. W. Raab, et al., "Lacritin rescues stressed epithelia via rapid forkhead box O3 (FOXO3)-associated autophagy that restores metabolism," J Biol Chem, vol. 288, no. 25, pp. 18146-18161, 2013.[3] T. Lin, R. Filek, J. M. 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Kim, et al., "Mitochondrial pathogenic mechanism and degradation in optineurin E50K mutation-mediated retinal ganglion cell degeneration," Sci Rep, vol. 6, pp. 33830, 2016.[12] M. J. Costello, L. A. Brennan, S. Basu, et al., "Autophagy and mitophagy participate in ocular lens organelle degradation," Exp Eye Res, vol. 116, pp. 141-150, 2013.[13] J. Zhou, K. Yao, Y. Zhang, et al., "Thioredoxin Binding Protein-2 Regulates Autophagy of Human Lens Epithelial Cells under Oxidative Stress via Inhibition of Akt Phosphorylation," vol. 2016, pp. 4856431, 2016.[14] K. A. Saadat, Y. Murakami, X. Tan, et al., "Inhibition of autophagy induces retinal pigment epithelial cell damage by the lipofuscin fluorophore A2E," FEBS Open Bio, vol. 4, pp. 1007-1014, 2014.[15] J. Zhang, Y. Bai, L. Huang, et al., "Protective effect of autophagy on human retinal pigment epithelial cells against lipofuscin fluorophore A2E: implications for age-related macular degeneration," Cell Death Dis, vol. 6, pp. e1972, 2015.[16] L. Perusek, B. Sahu, T. Parmar, et al., "Di-retinoid-pyridinium-ethanolamine (A2E) Accumulation and the Maintenance of the Visual Cycle Are Independent of Atg7-mediated Autophagy in the Retinal Pigmented Epithelium," J Biol Chem, vol. 290, no. 48, pp. 29035-29044, 2015.[17] A. Baek, S. Yoon, J. Kim, et al., "Autophagy and KRT8/keratin 8 protect degeneration of retinal pigment epithelium under oxidative stress," Autophagy, vol. 13, no. 2, pp. 248-263, 2017.[18] C. Song, S. K. Mitter, X. Qi, et al., "Oxidative stress-mediated NFkappaB phosphorylation upregulates p62/SQSTM1 and promotes retinal pigmented epithelial cell survival through increased autophagy," PLoS One, vol. 12, no. 2, pp. e0171940, 2017.[19] S. J. Sheu, J. L. Chen, Y. S. Bee, S. H. Lin and C. W. Shu, "ERBB2-modulated ATG4B and autophagic cell death in human ARPE19 during oxidative stress," PLoS One, vol. 14, no. 3, pp. e0213932, 2019.[20] I. Piano, E. Novelli, L. Della Santina, et al., "Involvement of Autophagic Pathway in the Progression of Retinal Degeneration in a Mouse Model of Diabetes," Front Cell Neurosci, vol. 10, pp. 42, 2016.[21] Jacqueline M.Lopes de Faria, Diego A. Duarte, Chiara Montemurro and A. Papadimitriou, "Defective Autophagy in Diabetic Retinopathy," 2016.[22] D. Fu, J. Y. Yu, S. Yang, et al., "Survival or death: a dual role for autophagy in stress-induced pericyte loss in diabetic retinopathy," Diabetologia, vol. 59, no. 10, pp. 2251-2261, 2016.[23] M. Ouimet and Y. L. Marcel, "Regulation of lipid droplet cholesterol efflux from macrophage foam cells," Arterioscler Thromb Vasc Biol, vol. 32, no. 3, pp. 575-581, 2012.[24] B. Razani, C. Feng, T. 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