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降低调节的miRNA-199a-5p通过激活ATF6信号通路而加剧甲诱导的心脏毒性

Wei Wang¹, Liang Dong², Hengxu Lv¹

¹Department of Oncology, The First Hospital of Hebei Medical University, Yuhua, Shijiazhuang 050031 Hebei, China.

|March 27, 2024

概括

甲 (5-FU) 化疗可以通过降低miRNA-199a-5p水平引起心脏损伤. 这会引发内质网膜压力,损害心脏细胞. 恢复miRNA-199a-5p可以防止这种心脏毒性.

科学领域:

心脏病学心脏病学
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

已知甲 (5-FU) 会引起严重的心脏毒性反应.
微RNA-199a-5p主要表达在心肌细胞中,对血管内皮有保护作用,并且在缺氧下下调,与心血管疾病相关.
这项研究调查了5-FU,miRNA-199a-5p和内分泌网膜应激在心脏毒性的联系.

研究的目的:

通过调节miRNA-199a-5p表达,探索5-FU是否通过激活内分泌网膜应激ATF6通路来诱导心脏毒性.
阐明5-FU诱导心脏毒性背后的分子机制.

主要方法:

主要的老鼠心肌细胞被用于体外研究与5-FU治疗.
研究了miRNA-199a-5p的表达及其调节作用在体外和体内.

主要成果:

5-FU治疗降低了心肌细胞中的miRNA-199a-5p表达.
这种降低激活了内质网膜应激ATF6通路,由增加的GRP78和ATF6表达证明,损害心肌细胞功能并诱导心脏毒性.
在救援试验中,用miRNA-199a-5p的补充证明了5-FU诱导的心脏毒性减少,这取决于降低ATF6信号通路的调节.

结论:

5-FU可以降低miRNA-199a-5p的表达.
这种下调激活了内分泌网膜应激ATF6通路,增加GRP78和ATF6,这会影响心肌细胞功能并导致心脏毒性.

关键词:

在ATF6信号通道中,心脏有毒性心脏有毒性甲是一种甲.微RNA-199a-5p 是一个小RNA.

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相关概念视频

MicroRNAs

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...