Updates on RPE cell damage in diabetic retinopathy (Review)
Diabetic retinopathy (DR) is a microvascular complication of diabetes. The retinal pigment epithelium (RPE) forms the outer layer of the blood-retinal barrier and serves a role in maintaining retinal function. RPE cell injury has been revealed in diabetic animal models, and high glucose (HG) levels...
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| Veröffentlicht in: | Molecular medicine reports 2023-10, Vol.28 (4), Article 185 |
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| creator | Li, Min Tian, Meimei Wang, Yuling Ma, Huijie Zhou, Yaru Jiang, Xinli Liu, Yan |
| description | Diabetic retinopathy (DR) is a microvascular complication of diabetes. The retinal pigment epithelium (RPE) forms the outer layer of the blood-retinal barrier and serves a role in maintaining retinal function. RPE cell injury has been revealed in diabetic animal models, and high glucose (HG) levels may cause damage to RPE cells by increasing the levels of oxidative stress, promoting pro-inflammatory gene expression, disrupting cell proliferation, inducing the endothelial-mesenchymal transition, weakening tight conjunctions and elevating cell death mechanisms, such as apoptosis, ferroptosis and pyroptosis. Non-coding RNAs including microRNAs, long non-coding RNAs and circular RNAs participate in RPE cell damage caused by HG levels, which may provide targeted therapeutic strategies for the treatment of DR. Plant extracts such as citrusin and hesperidin, and a number of hypoglycemic drugs, such as sodium-glucose co-transporter 2 inhibitors, metformin and glucagon-like peptide-1 receptor agonists, exhibit potential RPE protective effects; however, the detailed mechanisms behind these effects remain to be fully elucidated. An in-depth understanding of the contribution of the RPE to DR may provide novel perspectives and therapeutic targets for DR. |
| doi_str_mv | 10.3892/mmr.2023.13072 |
| format | Article |
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The retinal pigment epithelium (RPE) forms the outer layer of the blood-retinal barrier and serves a role in maintaining retinal function. RPE cell injury has been revealed in diabetic animal models, and high glucose (HG) levels may cause damage to RPE cells by increasing the levels of oxidative stress, promoting pro-inflammatory gene expression, disrupting cell proliferation, inducing the endothelial-mesenchymal transition, weakening tight conjunctions and elevating cell death mechanisms, such as apoptosis, ferroptosis and pyroptosis. Non-coding RNAs including microRNAs, long non-coding RNAs and circular RNAs participate in RPE cell damage caused by HG levels, which may provide targeted therapeutic strategies for the treatment of DR. Plant extracts such as citrusin and hesperidin, and a number of hypoglycemic drugs, such as sodium-glucose co-transporter 2 inhibitors, metformin and glucagon-like peptide-1 receptor agonists, exhibit potential RPE protective effects; however, the detailed mechanisms behind these effects remain to be fully elucidated. An in-depth understanding of the contribution of the RPE to DR may provide novel perspectives and therapeutic targets for DR.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2023.13072</identifier><language>eng</language><publisher>Athens: Spandidos Publications</publisher><subject>Animal models ; Apoptosis ; Cell adhesion & migration ; Cell death ; Cell growth ; Cell injury ; Cell proliferation ; Circular RNA ; Complications and side effects ; Cytokines ; Development and progression ; Diabetes ; Diabetes mellitus ; Diabetic retinopathy ; Drug development ; Epithelium ; Gene expression ; Genetic aspects ; GLP-1 receptor agonists ; Glucagon ; Glucagon-like peptide 1 ; Glucose transporter ; Health aspects ; Hesperidin ; Inflammation ; Kinases ; Metabolism ; Metformin ; MicroRNAs ; Microvasculature ; miRNA ; Mitochondria ; Non-coding RNA ; Oxidative stress ; Pathogenesis ; Physiological aspects ; Physiology ; Plant extracts ; Proteins ; Retina ; Retinal pigment epithelium ; Retinopathy ; RNA ; Therapeutic targets</subject><ispartof>Molecular medicine reports, 2023-10, Vol.28 (4), Article 185</ispartof><rights>COPYRIGHT 2023 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2023</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-d5663a35b316ec27deccf936cfe5e57a597788705a3e5eedf2cc50ee097365353</citedby><cites>FETCH-LOGICAL-c437t-d5663a35b316ec27deccf936cfe5e57a597788705a3e5eedf2cc50ee097365353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids></links><search><creatorcontrib>Li, Min</creatorcontrib><creatorcontrib>Tian, Meimei</creatorcontrib><creatorcontrib>Wang, Yuling</creatorcontrib><creatorcontrib>Ma, Huijie</creatorcontrib><creatorcontrib>Zhou, Yaru</creatorcontrib><creatorcontrib>Jiang, Xinli</creatorcontrib><creatorcontrib>Liu, Yan</creatorcontrib><title>Updates on RPE cell damage in diabetic retinopathy (Review)</title><title>Molecular medicine reports</title><description>Diabetic retinopathy (DR) is a microvascular complication of diabetes. The retinal pigment epithelium (RPE) forms the outer layer of the blood-retinal barrier and serves a role in maintaining retinal function. RPE cell injury has been revealed in diabetic animal models, and high glucose (HG) levels may cause damage to RPE cells by increasing the levels of oxidative stress, promoting pro-inflammatory gene expression, disrupting cell proliferation, inducing the endothelial-mesenchymal transition, weakening tight conjunctions and elevating cell death mechanisms, such as apoptosis, ferroptosis and pyroptosis. Non-coding RNAs including microRNAs, long non-coding RNAs and circular RNAs participate in RPE cell damage caused by HG levels, which may provide targeted therapeutic strategies for the treatment of DR. Plant extracts such as citrusin and hesperidin, and a number of hypoglycemic drugs, such as sodium-glucose co-transporter 2 inhibitors, metformin and glucagon-like peptide-1 receptor agonists, exhibit potential RPE protective effects; however, the detailed mechanisms behind these effects remain to be fully elucidated. An in-depth understanding of the contribution of the RPE to DR may provide novel perspectives and therapeutic targets for DR.</description><subject>Animal models</subject><subject>Apoptosis</subject><subject>Cell adhesion & migration</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Cell injury</subject><subject>Cell proliferation</subject><subject>Circular RNA</subject><subject>Complications and side effects</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic retinopathy</subject><subject>Drug development</subject><subject>Epithelium</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>GLP-1 receptor agonists</subject><subject>Glucagon</subject><subject>Glucagon-like peptide 1</subject><subject>Glucose transporter</subject><subject>Health aspects</subject><subject>Hesperidin</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Metabolism</subject><subject>Metformin</subject><subject>MicroRNAs</subject><subject>Microvasculature</subject><subject>miRNA</subject><subject>Mitochondria</subject><subject>Non-coding RNA</subject><subject>Oxidative stress</subject><subject>Pathogenesis</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Plant extracts</subject><subject>Proteins</subject><subject>Retina</subject><subject>Retinal pigment epithelium</subject><subject>Retinopathy</subject><subject>RNA</subject><subject>Therapeutic targets</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkU1LAzEQhhdRsFavngNe6mHXbLJJNngqpX5AQSn2HNLsbE3ZL5Ot0n9vVguClIGZYXjmnYE3iq5TnNBckru6dgnBhCYpxYKcRKNUyDSmGGenh55IKc6jC--3GHNGmBxF96uu0D141DZo-TpHBqoKFbrWG0C2QYXVa-itQS7kpu10_75HkyV8Wvi6vYzOSl15uDrUcbR6mL_NnuLFy-PzbLqITUZFHxeMc6opW9OUgyGiAGNKSbkpgQETmkkh8lxgpmkYQFESYxgGwFJQziij42jyq9u59mMHvle19cOjuoF25xXJGZUZ55IH9OYfum13rgnfBYrLlNGMsz9qoytQtinb3mkziKqp4DkOlzkJVHKEClFAbU3bQGnD_NiCca33DkrVOVtrt1cpVoNFKlikBovUj0X0G4WugLY</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Li, Min</creator><creator>Tian, Meimei</creator><creator>Wang, Yuling</creator><creator>Ma, Huijie</creator><creator>Zhou, Yaru</creator><creator>Jiang, Xinli</creator><creator>Liu, Yan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20231001</creationdate><title>Updates on RPE cell damage in diabetic retinopathy (Review)</title><author>Li, Min ; 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The retinal pigment epithelium (RPE) forms the outer layer of the blood-retinal barrier and serves a role in maintaining retinal function. RPE cell injury has been revealed in diabetic animal models, and high glucose (HG) levels may cause damage to RPE cells by increasing the levels of oxidative stress, promoting pro-inflammatory gene expression, disrupting cell proliferation, inducing the endothelial-mesenchymal transition, weakening tight conjunctions and elevating cell death mechanisms, such as apoptosis, ferroptosis and pyroptosis. Non-coding RNAs including microRNAs, long non-coding RNAs and circular RNAs participate in RPE cell damage caused by HG levels, which may provide targeted therapeutic strategies for the treatment of DR. Plant extracts such as citrusin and hesperidin, and a number of hypoglycemic drugs, such as sodium-glucose co-transporter 2 inhibitors, metformin and glucagon-like peptide-1 receptor agonists, exhibit potential RPE protective effects; however, the detailed mechanisms behind these effects remain to be fully elucidated. An in-depth understanding of the contribution of the RPE to DR may provide novel perspectives and therapeutic targets for DR.</abstract><cop>Athens</cop><pub>Spandidos Publications</pub><doi>10.3892/mmr.2023.13072</doi></addata></record> |
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| subjects | Animal models Apoptosis Cell adhesion & migration Cell death Cell growth Cell injury Cell proliferation Circular RNA Complications and side effects Cytokines Development and progression Diabetes Diabetes mellitus Diabetic retinopathy Drug development Epithelium Gene expression Genetic aspects GLP-1 receptor agonists Glucagon Glucagon-like peptide 1 Glucose transporter Health aspects Hesperidin Inflammation Kinases Metabolism Metformin MicroRNAs Microvasculature miRNA Mitochondria Non-coding RNA Oxidative stress Pathogenesis Physiological aspects Physiology Plant extracts Proteins Retina Retinal pigment epithelium Retinopathy RNA Therapeutic targets |
| title | Updates on RPE cell damage in diabetic retinopathy (Review) |
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