Cldn10a in kidney injury susceptibility (A07 (C06))

Cldn10a 与肾损伤易感性的关系 (A07 (C06))

• 批准号: 516826087
• 金额: --
• 依托单位: Klinik für Nieren- und Hochdruckerkrankungen
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2023
• 资助国家: 德国
• 起止时间: 2022-12-31 至 无数据
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/516826087?language=en
• 关键词: Cldn10a; kidney; injury; susceptibility; A07

Project A07 will investigate the role of tight junction constituents in acute kidney injury (AKI) and the tight junction regulome as a potential target for renoprotection. We will focus on the proximal tubule (PT)-specific paracellular Cl- channel Cldn10a, testing the hypotheses that Cldn10a is critical for PT cell energy expenditure and that its upregulation at later phases after AKI confers renoprotection from future insults. Single cell multi-omics will be employed to unveil gene expression regulation of Cldn10a and other tight junction components in healthy kidney and in AKI. We will utilize a single cell CRISPRi screen to identify critical upstream regulators of PT tight junction biogenesis, which might constitute actionable targets for renoprotection.

项目A07将研究紧密连接组分在急性肾损伤（阿基）中的作用，以及紧密连接调节组作为肾保护的潜在靶点。我们将集中在近端小管（PT）特异性的细胞旁氯离子通道Cldn10a，测试的假设，Cldn10a是PT细胞能量消耗的关键，它的上调后，阿基赋予肾保护从未来的侮辱后期阶段。单细胞多组学将用于揭示健康肾脏和阿基中Cldn10a和其他紧密连接组分的基因表达调控。我们将利用单细胞CRISPRi筛选来鉴定PT紧密连接生物发生的关键上游调节因子，这可能构成肾保护的可操作靶点。