{"title":"通过 miR-196a-5p/CALM3 轴激活 ERK 通路，沉默 circRUFY1 保护急性眼内高压症中的视网膜神经节细胞损伤","authors":"BinBin Li, ShaoJun Li, Wei Tang, Min Zeng","doi":"10.1007/s13273-024-00469-z","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Neuroinflammation has been recognized as a key pathological event in acute glaucoma. Medical treatment of acute glaucoma has mainly focused on lowering intraocular pressure, yet the majority of patients still experience deterioration. Aberrant expression or activity of circular RNAs in the retina has been described in various ophthalmic diseases.</p><h3 data-test=\"abstract-sub-heading\">Objective</h3><p>This study surveyed the mechanism of circRUFY1 in acute ocular hypertension (AOH)-induced retinal ganglion cell (RGC) injury.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>AOH rats expressed high circRUFY1 and CALM3, and low miR-196a-5p in the retina tissue. CircRUFY1 silencing in AOH-induced rats reduced the severity of retinal damage and RGC damage. CircRUFY1, as a ceRNA of miR-196a-5p, upregulated CALM3, and CALM3 overexpression could further activate the ERK pathway signaling in RGCs.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>Silence of circRUFY1 protects RGCs from AOH injury mainly by inhibiting the ERK signaling pathway by regulating the miR-196a-5p/CALM3 axis. Overall, targeted intervention of circRUFY1 expression is a promising therapeutic strategy for treating RGC damage in acute glaucoma.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"11 1","pages":""},"PeriodicalIF":1.1000,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Silencing circRUFY1 protects retinal ganglion cell injury in acute intraocular hypertension by activating the ERK pathway through miR-196a-5p/CALM3 axis\",\"authors\":\"BinBin Li, ShaoJun Li, Wei Tang, Min Zeng\",\"doi\":\"10.1007/s13273-024-00469-z\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<h3 data-test=\\\"abstract-sub-heading\\\">Background</h3><p>Neuroinflammation has been recognized as a key pathological event in acute glaucoma. Medical treatment of acute glaucoma has mainly focused on lowering intraocular pressure, yet the majority of patients still experience deterioration. Aberrant expression or activity of circular RNAs in the retina has been described in various ophthalmic diseases.</p><h3 data-test=\\\"abstract-sub-heading\\\">Objective</h3><p>This study surveyed the mechanism of circRUFY1 in acute ocular hypertension (AOH)-induced retinal ganglion cell (RGC) injury.</p><h3 data-test=\\\"abstract-sub-heading\\\">Results</h3><p>AOH rats expressed high circRUFY1 and CALM3, and low miR-196a-5p in the retina tissue. CircRUFY1 silencing in AOH-induced rats reduced the severity of retinal damage and RGC damage. CircRUFY1, as a ceRNA of miR-196a-5p, upregulated CALM3, and CALM3 overexpression could further activate the ERK pathway signaling in RGCs.</p><h3 data-test=\\\"abstract-sub-heading\\\">Conclusion</h3><p>Silence of circRUFY1 protects RGCs from AOH injury mainly by inhibiting the ERK signaling pathway by regulating the miR-196a-5p/CALM3 axis. Overall, targeted intervention of circRUFY1 expression is a promising therapeutic strategy for treating RGC damage in acute glaucoma.</p>\",\"PeriodicalId\":18683,\"journal\":{\"name\":\"Molecular & Cellular Toxicology\",\"volume\":\"11 1\",\"pages\":\"\"},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2024-07-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & Cellular Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s13273-024-00469-z\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & Cellular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s13273-024-00469-z","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"TOXICOLOGY","Score":null,"Total":0}
Silencing circRUFY1 protects retinal ganglion cell injury in acute intraocular hypertension by activating the ERK pathway through miR-196a-5p/CALM3 axis
Background
Neuroinflammation has been recognized as a key pathological event in acute glaucoma. Medical treatment of acute glaucoma has mainly focused on lowering intraocular pressure, yet the majority of patients still experience deterioration. Aberrant expression or activity of circular RNAs in the retina has been described in various ophthalmic diseases.
Objective
This study surveyed the mechanism of circRUFY1 in acute ocular hypertension (AOH)-induced retinal ganglion cell (RGC) injury.
Results
AOH rats expressed high circRUFY1 and CALM3, and low miR-196a-5p in the retina tissue. CircRUFY1 silencing in AOH-induced rats reduced the severity of retinal damage and RGC damage. CircRUFY1, as a ceRNA of miR-196a-5p, upregulated CALM3, and CALM3 overexpression could further activate the ERK pathway signaling in RGCs.
Conclusion
Silence of circRUFY1 protects RGCs from AOH injury mainly by inhibiting the ERK signaling pathway by regulating the miR-196a-5p/CALM3 axis. Overall, targeted intervention of circRUFY1 expression is a promising therapeutic strategy for treating RGC damage in acute glaucoma.
期刊介绍：
Molecular & Cellular Toxicology publishes original research and reviews in all areas of the complex interaction between the cell´s genome (the sum of all genes within the chromosome), chemicals in the environment, and disease. Acceptable manuscripts are the ones that deal with some topics of environmental contaminants, including those that lie in the domains of analytical chemistry, biochemistry, pharmacology and toxicology with the aspects of molecular and cellular levels. Emphasis will be placed on toxic effects observed at relevant genomics and proteomics, which have direct impact on drug development, environment health, food safety, preventive medicine, and forensic medicine. The journal is committed to rapid peer review to ensure the publication of highest quality original research and timely news and review articles.
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