时间标签：数据日期 2026-11-03 · 生成时间 2026-11-03 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31 – 2026/11/03 ｜ 情报发生日期 2026-11-03
研究问题
These studies underscore the critical need to investigate whether exosomal KLF3‐AS1 regulates microglial polarisation in CIRI, which will provide essential experimental evidence for translating BMSC‐derived exosome‐based therapies into clinical practice.；Although prior studies have demonstrated that BMSC‐derived exosomal KLF3‐AS1 exerts neuroprotective effects against CIRI through two distinct SIRT1‐related mechanisms, whether KLF3‐AS1 regulates microglial mitochondrial function and inflammatory polarisation through SIRT3, a NAD + ‐dependent deacetylase primarily localised in mitochondria and critically involved in metabolic regulation, remains unknown.；Moreover, the epigenetic regulation of KLF3‐AS1 expression in BMSCs has not been explored.
方法
Cells were maintained at 37°C in a humidified incubator with 5% CO 2 .；15 Briefly, mice were anaesthetised, and bone marrow cells were flushed and centrifuged at 1000 rpm for 5 min to pellet cells.；Cells were then cultured in Dulbecco's Modified Eagle Medium (DMEM)/10% fetal bovine serum (FBS, Thermo Fisher Scientific) under standard conditions (37°C, 5% CO 2 ).
核心结论
15 These findings suggest that upregulating KLF3‐AS1 expression in BMSC‐derived exosomes represents a potential therapeutic strategy for CIRI.；Here, we found that the histone acetylation and demethylation at the KLF3‐AS1 promoter synergistically upregulate KLF3‐AS1 expression in BMSC‐derived exosomes, thereby enhancing BMSC migration and functionality.；We found that overexpression of KLF3‐AS1 increased BMSC viability (Figure 1E ).
局限
However, the complex pathogenesis of CIRI has hindered the development of effective therapeutic approaches.；19 , 20 However, whether ETV4 mediates KLF3‐AS1‐induced microglial mitochondrial regulation and inflammatory polarisation remains unexplored.
对本项目的价值
中等价值：属「表观遗传时钟与生物学年龄读数」方向；线粒体功能与氧化应激栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.9/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 69,060 字符，题名指纹 0.81，已过 DOI 逐字 + 题名指纹 + 正文长度三重归属校验）
原文题录
- 中文题名：核内 KLF3-AS1 经组蛋白乙酰化/甲基化平衡保护小胶质线粒体功能，减轻脑缺血再灌注损伤
- 英文标题：Intranuclear localisation of KLF3-AS1 under the balance of histone acetylation and methylation in BMSCs ameliorates cerebral ischaemia‒reperfusion injury by preserving microglial mitochondrial function and inhibiting inflammatory polarisation.
- 期刊与标识：Clin Transl Med · PMID 42965486 · DOI 10.1002/ctm2.70870 · PMC PMC13723223 · EDAT 2026-10-31