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准内质网膜压力诱导的淋巴功能障碍,以减轻与双酸相关的骨髓缩

Ziyue Qin^1,2, Hanyu Xie^1,2, Pengcheng Su^1,2

¹Department of Oral and Maxillofacial Surgery, The Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing, China.

Clinical and translational medicine

|November 9, 2024

概括

与双酸盐相关的下巴骨 necrosis (BRONJ) 涉及淋巴排水受损. 索莱德酸会引起淋巴细胞内质网膜应激和亡,但一种新的纳米粒子疗法恢复了淋巴功能并减轻了BRONJ.

科学领域:

生物医学研究的研究.
细胞生物学细胞生物学
病理学病理学病理学

背景情况:

双酸盐 (BPs) 对于治疗骨质再吸收障碍至关重要.
双酸盐相关的骨亡 (BRONJ) 是一种严重的并发症,其特征是炎症和骨亡.
淋巴疏通障碍在BRONJ病变发生中的作用尚不清楚.

研究的目的:

为了研究受损淋巴排水对BRONJ的影响.
阐明勒酸 (ZA) 诱导的淋巴内皮细胞 (LEC) 损伤背后的机制.
评估一种新的纳米粒子疗法,以缓解BRONJ.

主要方法:

建立了BRONJ的小鼠模型来评估淋巴功能.
使用了组织清除,淋巴清除测定,流细胞计和组织病理学.
采用RNA测序,代谢学,电子显微镜和西方涂抹来分析ZA对LEC的影响.
生成了条件淘汰赛小鼠来研究SIRT6和ATG5.5的作用.
开发并测试了纳米粒子载荷的ZA和拉巴胺素 (ZDPR) 用于BRONJ处理.

主要成果:

青铜模型表现出淋巴疏通受损,炎症和骨亡.
ZA诱导了内等质网膜应激 (ERS) 和抑制了LEC中的自,导致了亡.
ZA激活了NAD+/SIRT6/XBP1s通路,导致LEC中的ERS诱导的亡.
删除SIRT6或ATG5在BRONJ中加剧了淋巴功能障碍和炎症.
ZDPR纳米颗粒减轻了LEC中的ERS-亡,改善了淋巴功能,解决了炎症.

结论:

在ZA治疗的LEC中,NAD+/SIRT6/XBP1s通路调解了ERS诱导的亡.
淋巴排水障碍加剧了.
ZDPR纳米颗粒通过恢复内皮功能和淋巴排水来显示治疗潜力,有效地减轻BRONJ.

关键词:

自自是自的过程.双酸盐是一种双酸盐.细胞内膜网膜的压力应激淋巴排水系统的淋巴排水.骨质结核病的结核病.

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