急性和慢性病的共享多细胞损伤计划使机械患者分层成为可能
medRxiv : the preprint server for health sciences
|March 13, 2026
概括
急性损伤 (AKI) 和慢性病 (CKD) 具有共同的分子机制,由单核转录学揭示出来. 这些发现将损伤分子程序与预测患者结果的非侵入性蛋白质特征联系起来.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 基因组学就是基因组学.
- 分子生物学分子生物学
背景情况:
- 急性损伤 (AKI) 和慢性病 (CKD) 是不同的,但相互关联的疾病,具有复杂的临床轨迹.
- 转录组学的最新进展为健康和疾病中的细胞多样性提供了洞察力.
研究的目的:
- 在AKI和CKD患者的活检中研究分子多样性和共同点,使用单核转录学.
- 识别导致急性和慢性损伤的共同分子机制.
主要方法:
- 在精密医学项目 (KPMP) 的150多个脏活检中采用单核转录学.
- 利用无监督的方法来识别与急性损伤和慢性损伤相关的多细胞程序.
- 将分子程序映射到尿液和血蛋白质配置文件,并在英国生物银行得到验证.
主要成果:
- 确定了两种与急性损伤和慢性损伤相关的独特的多细胞程序,在AKI和CKD患者中表现出来.
- 揭示了AKI和CKD的共同分子机制,而不是不同的途径.
- 发现这些分子程序反映了管状上皮细胞修复状态和细胞应激.
- 确定NFkB,AP-1和STAT家族成员作为潜在的上游监管机构.
- 建立了分子损伤特征和预测结局的非侵入性蛋白质概况之间的联系.
结论:
- 在病中对细胞程序的公正识别为AKI和CKD的损伤机制提供了统一的观点.
- 从分子数据中获得的非侵入性蛋白质签名可以预测长期的结局.
- 这项研究通过将分子见解与临床轨迹和患者结果联系起来,推动了精准医学的发展.
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