cFLIPL通过调节热致死来缓解心肌缺血-再输液损伤
Dong Zhang1,2, Hui Wu1,2, Di Liu1,2
1Institute of Cardiovascular Disease, China Three Gorges University, Yichang, China.
Cell biology international
|September 26, 2023
概括
细胞FLIP-Long (cFLIP L) 过度表达通过抑制热致死,可以防止心肌缺血-反损伤 (MIRI). 这一发现表明cFLIP是心脏病发作恢复的潜在治疗标.
科学领域:
- 心脏病学 心脏病学
- 细胞生物学 细胞生物学
- 分子医学是分子医学.
背景情况:
- 心肌缺血-反损伤 (MIRI) 在急性心肌梗塞后显著影响心脏功能.
- 炎症性细胞死亡的热,越来越多地被认为是MIRI病变发生的关键调节者.
研究的目的:
- 为了研究细胞FLIP-Long (cFLIP L) 在MIRI中的作用.
- 为了确定cFLIP是否可以调节热和保护MIRI.
主要方法:
- 建立了体外 (H9c2细胞) 和体内 (SD大鼠) 的缺血-再输液 (I/R) 和缺氧-再氧化 (H/R) 损伤模型.
- 用于cFLIPL过度表达的复合腺病毒载体.
- 评估了烧亡标志物 (ASC,Caspase 1,NLRP3,GSDMD-N,IL-1β,IL-18) 和细胞活力.
主要成果:
- 缺血/反和低氧/低氧化显著减少了内源性cFLIPL表达.
- 过度表达cFLIPL抑制了热,减少了大鼠心肌梗塞的大小,并改善了H9c2细胞活力.
- I/R和H/R损伤高调关键的灭与灭相关的蛋白质和诱导细胞灭.
结论:
- cFLIP通过抑制 pyroptotic 途径在 MIRI 中发挥保护作用.
- cFLIP可能通过与Caspase 1相互作用来发挥其作用,从而减少炎症性细胞因子的释放,并防止细胞膜损伤.
- cFLIP L 是一个有希望的治疗点,可以缓解MIRI.
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