Toru Hosoi, J. Nomura, Keigo Tanaka, K. Ozawa, A. Nishi, Y. Nomura
{"title":"内质网应激与神经退行性疾病自噬的关系","authors":"Toru Hosoi, J. Nomura, Keigo Tanaka, K. Ozawa, A. Nishi, Y. Nomura","doi":"10.1515/ersc-2017-0004","DOIUrl":null,"url":null,"abstract":"Abstract Increasing evidence suggests that endoplasmic reticulum (ER) stress and autophagy play an important role in regulating brain function. ER stress activates three major branches of the unfolded protein response (UPR) pathways, namely inositol-requiring enzyme-1 (IRE1), double stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK) and activating transcription factor 6 (ATF6)-mediated pathways. Recent studies have suggested that these UPR signals may be linked to autophagy. In this review article, we summarize recent evidence and discuss a possible link between ER stress and autophagy with regard to neurodegenerative diseases. Furthermore, possible pharmacological strategies targeting UPR and autophagy are discussed.","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":"46 1","pages":"37 - 45"},"PeriodicalIF":0.7000,"publicationDate":"2017-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"7","resultStr":"{\"title\":\"Link between endoplasmic reticulum stress and autophagy in neurodegenerative diseases\",\"authors\":\"Toru Hosoi, J. Nomura, Keigo Tanaka, K. Ozawa, A. Nishi, Y. Nomura\",\"doi\":\"10.1515/ersc-2017-0004\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Abstract Increasing evidence suggests that endoplasmic reticulum (ER) stress and autophagy play an important role in regulating brain function. ER stress activates three major branches of the unfolded protein response (UPR) pathways, namely inositol-requiring enzyme-1 (IRE1), double stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK) and activating transcription factor 6 (ATF6)-mediated pathways. Recent studies have suggested that these UPR signals may be linked to autophagy. In this review article, we summarize recent evidence and discuss a possible link between ER stress and autophagy with regard to neurodegenerative diseases. Furthermore, possible pharmacological strategies targeting UPR and autophagy are discussed.\",\"PeriodicalId\":29730,\"journal\":{\"name\":\"Cell Pathology\",\"volume\":\"46 1\",\"pages\":\"37 - 45\"},\"PeriodicalIF\":0.7000,\"publicationDate\":\"2017-11-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Pathology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1515/ersc-2017-0004\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Pathology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1515/ersc-2017-0004","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Link between endoplasmic reticulum stress and autophagy in neurodegenerative diseases
Abstract Increasing evidence suggests that endoplasmic reticulum (ER) stress and autophagy play an important role in regulating brain function. ER stress activates three major branches of the unfolded protein response (UPR) pathways, namely inositol-requiring enzyme-1 (IRE1), double stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK) and activating transcription factor 6 (ATF6)-mediated pathways. Recent studies have suggested that these UPR signals may be linked to autophagy. In this review article, we summarize recent evidence and discuss a possible link between ER stress and autophagy with regard to neurodegenerative diseases. Furthermore, possible pharmacological strategies targeting UPR and autophagy are discussed.