心肌梗塞中的基因素脱乙酶:编排已编程的细胞死亡途径和新兴的治疗机会
Huai Wen1, Marady Hun1, Qiong He2
1Department of Pediatrics, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, China.
概括
基因组脱乙酶 (HDACs) 调节心脏病发作后编程细胞死亡 (PCD) 途径. 了解异形特异性作用为心肌梗塞 (MI) 提供了新的治疗策略.
科学领域:
- 心血管生物学 心血管生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 细胞死亡研究 细胞死亡研究
背景情况:
- 心肌梗塞 (MI) 通过多种编程细胞死亡 (PCD) 途径导致不可逆转的心肌细胞损失.
- 基因组脱乙酶 (HDACs) 是关键的表观遗传调节剂,影响PCD,炎症和心脏重塑后MI.
- HDAC异型在促进或抑制心肌细胞死亡方面具有复杂的,取决于环境的作用.
研究的目的:
- 系统地审查最近关于异形特异性HDAC在MI期间调节不同PCD通路中的角色的进展.
- 突出HDACs在心肌损伤中的机械复杂性和治疗潜力.
- 批判性地评估新兴的临床前策略,针对针对心脏病发作治疗的HDAC.
主要方法:
- 对临床前和临床研究的系统文献综述.
- 对将HDAC与特定PCD途径 (亡,亡,自,铁亡,热亡) 联系起来的分子机制的分析.
- 针对HDACs的治疗干预措施的评估,包括抑制剂和激活剂.
主要成果:
- HDACs调节组织蛋白和非组织蛋白的乙化,影响心肌细胞的存活和死亡.
- 异形特异性HDACs差异调节各种PCD途径,影响心肌损伤和炎症.
- 临床前研究表明,HDAC抑制剂和激活剂在保证心脏功能后的MI.
结论:
- 解读异形特异性HDAC介导的心肌细胞PCD调节对于理解MI至关重要.
- 针对特定的HDACs提供了有前途的治疗途径,以保持心肌完整性和改善心肌梗塞后的结果.
- 对HDAC向疗法的转化前景进行进一步的研究是必要的,以获得临床应用.
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