Dickkopf-3 (DKK3) as a mediator of cardiorenal injury (C10*)

Dickkopf-3 (DKK3) 作为心肾损伤的介质 (C10*)

• 批准号: 497114503
• 金额: --
• 依托单位: Klinik für Innere Medizin IV - Nieren- und Hochdruckkrankheiten
• 依托单位国家: 德国
• 项目类别: CRC/Transregios
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/497114503?language=en
• 关键词: Dickkopf; DKK3; mediator; cardiorenal; injury

Tissue fibrosis represents a hallmark of advanced CKD and CVD leading to final organ failure. Recent experimental work in various CKD models has documented the crucial involvement of the Wnt/β-catenin pathway in the development of tubulointerstitial fibrosis and thus progressive CKD. Dickkopf-3 (DKK3) is a member of the Dickkopf protein family, which is closely involved in the regulation of the Wnt/β-catenin signaling. This project aims to systematically dissect the impact of DKK3 on cardiorenal injury and to assess on whether modulation of DKK3 may provide a specific therapeutic target in the management of CKD and its cardiovascular complications.

组织纤维化是晚期 CKD 和 CVD 导致最终器官衰竭的标志。最近在各种 CKD 模型中的实验工作证明了 Wnt/β-catenin 通路在肾小管间质纤维化以及进展性 CKD 发展中的重要作用。 Dickkopf-3 (DKK3) 是 Dickkopf 蛋白家族的成员，与 Wnt/β-catenin 信号传导密切相关。该项目旨在系统剖析 DKK3 对心肾损伤的影响，并评估 DKK3 的调节是否可以为 CKD 及其心血管并发症的治疗提供特定的治疗靶点。