研究进展 情报发生 2026-10-31 · 发布于 2026-11-01

五味子乙素经 CTR1 抑制铜死亡:减轻缺血性急性肾损伤的机制

来源:Front Cell Dev Biol · PMID 42959219 · DOI 10.3389/fcell.2026.1993380 · 来源:IMA 知识库《文献层·文献监控卡片》2026-10-31 期 · 全文级(file_id dmlmcfQeUyzO,实际下载核验) · 全文已获取并通过归属校验

时间标签:数据日期 2026-10-31 · 生成时间 2026-11-01 05:30(Asia/Shanghai)| 检索窗口 PubMed edat 2026/10/28–2026/10/31 | 情报发生日期 2026-10-31

研究问题

Acute kidney injury (AKI) affects 13.3 million individuals annually worldwide, with a mortality rate exceeding 50% in critically ill patients.;Despite advances in supportive care, no targeted pharmacotherapies are available.

方法

Successful transfection was validated using western blot analysis.;Lactate dehydrogenase (LDH) release, a marker of cell membrane damage, was quantified using an LDH Cytotoxicity Assay Kit (Beyotime, Shanghai, China).;The LDH assay signal was assessed by recording the absorbance at 490 nm.;Animal procedures were approved by the Institutional Animal Care and Use Committee (IACUC) of Chongqing Medical University (approval no.

核心结论

Compared with the sham-operated control group, the proportion of cuproptosis increased significantly after ischemic injury ().;GO analysis revealed significant enrichment of cuproptosis-related biological processes after I/R injury, particularly those involving oxidative stress responses, cell-cell signaling by Wnt, regulation of Wnt signaling, stress-activated MAPK cascade, JAK-STAT ().;KEGG pathway analysis highlighted metal ion homeostasis and MAPK signaling as the most significantly altered pathways (), implicating copper-redox dysregulation in AKI pathogenesis. ‖ 结论:These findings provide a preclinical rationale for the repurposing of this natural product for the treatment of ischemic kidney disease.

局限

Third, these findings provide a preclinical rationale for strategies aimed at preserving physiological copper function and limiting pathological copper accumulation.;A limitation of our single-cell gene-set scoring approach is its inability to distinguish baseline metabolic gene expression from active cell death program activation.;Future studies employing orthogonal approaches—such as assessing DLAT oligomerization, iron-sulfur cluster protein stability, and FDX1-dependent functional rescue assays—are needed to differentiate cuproptosis execution from a state of copper susceptibility.

对本项目的价值

★☆☆☆☆ 代谢轴既干预敏感性最高,也是老药新用供给最充足的来源。设计 single-cell。

全文来源

PMC JATS 全文(正文 39,630 字符,已过标题/DOI 逐字归属校验)

原文题录

  • 英文标题:Schisandrin B attenuates ischemic acute kidney injury in a CTR1-dependent manner by inhibiting cuproptosis.
  • 期刊与标识:Front Cell Dev Biol · PMID 42959219 · DOI 10.3389/fcell.2026.1993380

A 级证据分级:A 级(同行评议人体研究)

本文属人体研究证据,但需注意:观察性或小样本干预的结论不等于已证实临床获益;效应量与长期安全性仍需更大规模、更长随访的试验验证。

关于本文的文献来源:本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写,依据已获取的期刊全文(方法、样本量与结论已回到原文核对);未能获取全文的同批条目另行标注「摘要级」,全程未做任何数值推算补全。