心脏代谢和抗高血糖药物的心脏调节作用:氧化和内质网膜应激作用的作用
1Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Florida Jacksonville College of Medicine, 653-1 West 8th Street, Jacksonville, FL, 32209, USA. arshag.mooradian@jax.ufl.edu.
概括
糖尿病并发症如高血糖和低血糖导致细胞应激,增加心血管风险. 新的糖尿病药物可以通过减少这种压力来保护心脏.
科学领域:
- 心脏病学 心脏病学
- 内分泌学 在内分泌学.
- 细胞生物学 细胞生物学
背景情况:
- 失控的糖尿病,标志着高血糖和低血糖,增加了心血管疾病 (CVD) 的风险.
- 高血糖和低血糖都会诱导细胞应激,特别是内质网膜 (ER) 应激,这是已知的心血管疾病促进者.
研究的目的:
- 审查细胞减压在现代糖尿病药物的心脏保护作用中的作用.
- 探索细胞压力是心血管疾病的关键因素的假设.
主要方法:
- 文献综述侧重于当代抗高血糖药物和其他心脏保护剂的作用机制.
- 对研究的分析,研究高血糖,低血糖和药物干预对细胞应激通路 (氧化和ER压力) 的影响.
主要成果:
- 类似葡萄糖类1 (GLP-1) 受体激动剂和-葡萄糖共运输体2 (SGLT-2) 抑制剂可减少人类冠状动脉内皮细胞中的氧化和ER压力.
- 心脏保护药物,如他类药物和氨酸-血管酶-氨系统 (RAAS) 抑制剂,也表现出细胞减压效应.
- 抗氧化剂可能会加剧ER压力,可能解释不良的临床试验结果.
结论:
- 减少细胞压力是当代糖尿病药物的心脏保护益处的潜在机制.
- 需要进一步的临床试验来证实细胞应激在心血管疾病发病和管理中的中心作用.
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