{"title":"单细胞技术对急性肾损伤和向慢性肾脏疾病过渡的见解。","authors":"Benjamin D Humphreys","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Outcomes after acute kidney injury (AKI) cover a wide spectrum ranging from full recovery to incomplete repair leading to transition to chronic kidney disease (CKD). This \"AKI to CKD transition\" is incompletely understood at a cellular level and there is a pressing need to identify the basic mechanisms of successful recovery from AKI and to develop therapeutic interventions to prevent the AKI to CKD transition. In recent years, single-cell transcriptomic and epigenomic technologies have substantially improved our understanding of cell types and states in homeostasis and after injury. In this paper, I will review our recent work applying single-cell technologies to better understand AKI and its transition to CKD, focusing on a proximal tubule cell state that we have termed \"failed repair.\" Failed repair proximal tubule cells are characterized by pro-inflammatory and pro-fibrotic gene expression patterns and may drive the AKI to CKD transition.</p>","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"383-392"},"PeriodicalIF":0.0000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323478/pdf/","citationCount":"0","resultStr":"{\"title\":\"INSIGHTS INTO ACUTE KIDNEY INJURY AND TRANSITION TO CHRONIC KIDNEY DISEASE BY SINGLE-CELL TECHNOLOGIES.\",\"authors\":\"Benjamin D Humphreys\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Outcomes after acute kidney injury (AKI) cover a wide spectrum ranging from full recovery to incomplete repair leading to transition to chronic kidney disease (CKD). This \\\"AKI to CKD transition\\\" is incompletely understood at a cellular level and there is a pressing need to identify the basic mechanisms of successful recovery from AKI and to develop therapeutic interventions to prevent the AKI to CKD transition. In recent years, single-cell transcriptomic and epigenomic technologies have substantially improved our understanding of cell types and states in homeostasis and after injury. In this paper, I will review our recent work applying single-cell technologies to better understand AKI and its transition to CKD, focusing on a proximal tubule cell state that we have termed \\\"failed repair.\\\" Failed repair proximal tubule cells are characterized by pro-inflammatory and pro-fibrotic gene expression patterns and may drive the AKI to CKD transition.</p>\",\"PeriodicalId\":23186,\"journal\":{\"name\":\"Transactions of the American Clinical and Climatological Association\",\"volume\":\"135 \",\"pages\":\"383-392\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323478/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Transactions of the American Clinical and Climatological Association\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Transactions of the American Clinical and Climatological Association","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
INSIGHTS INTO ACUTE KIDNEY INJURY AND TRANSITION TO CHRONIC KIDNEY DISEASE BY SINGLE-CELL TECHNOLOGIES.
Outcomes after acute kidney injury (AKI) cover a wide spectrum ranging from full recovery to incomplete repair leading to transition to chronic kidney disease (CKD). This "AKI to CKD transition" is incompletely understood at a cellular level and there is a pressing need to identify the basic mechanisms of successful recovery from AKI and to develop therapeutic interventions to prevent the AKI to CKD transition. In recent years, single-cell transcriptomic and epigenomic technologies have substantially improved our understanding of cell types and states in homeostasis and after injury. In this paper, I will review our recent work applying single-cell technologies to better understand AKI and its transition to CKD, focusing on a proximal tubule cell state that we have termed "failed repair." Failed repair proximal tubule cells are characterized by pro-inflammatory and pro-fibrotic gene expression patterns and may drive the AKI to CKD transition.