单细胞技术对急性肾损伤和向慢性肾脏疾病过渡的见解。

Q2 Medicine
Benjamin D Humphreys
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引用次数: 0

摘要

急性肾损伤(AKI)后的结果涵盖范围很广,从完全恢复到不完全修复,从而过渡到慢性肾脏疾病(CKD)。这种“AKI向CKD过渡”在细胞水平上尚不完全清楚,迫切需要确定AKI成功恢复的基本机制,并制定治疗干预措施以防止AKI向CKD过渡。近年来,单细胞转录组学和表观基因组学技术极大地提高了我们对稳态和损伤后细胞类型和状态的理解。在本文中,我将回顾我们最近应用单细胞技术来更好地理解AKI及其向CKD过渡的工作,重点关注我们称之为“失败修复”的近端小管细胞状态。修复失败的近端小管细胞具有促炎和促纤维化基因表达模式的特征,并可能驱动AKI向CKD过渡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

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CiteScore
1.70
自引率
0.00%
发文量
57
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