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气体信号分子SO₂对甲状腺功能高大鼠心脏功能的影响

Qi Yang¹, Ting Yang², Xing Liu¹

¹Department of Cardiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang 421000, Hunan, China.

The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology

|February 28, 2024

概括

二氧化硫 (SO2) 可以通过减少亡和纤维化来预防甲状腺功能过高引起的心肌病. 这种气体信号分子为治疗甲状腺功能过高患者心脏病提供了潜在的新策略.

科学领域:

心血管生物学心血管生物学
内分泌学在内分泌学.
气体传递器信号传输

背景情况:

甲状腺功能障碍引起的心肌病 (HTC) 涉及心肌纤维化,导致心脏功能和预后不佳.
肌心纤维化主要是由亡和内质网膜应激 (ERS) 驱动的.
二氧化硫 (SO2),一种内源气体,在调节心脏功能方面发挥作用.

研究的目的:

研究SO2对甲状腺功能过高引起的心肌纤维化的治疗作用.
阐明潜在的机制,包括ERS,亡和Hippo路径的参与.

主要方法:

在实验室和体内实验中,使用甲状腺功能过高的老鼠模型进行实验.
评估了心肌间歇性原沉积 (马森染色).
通过ELISA,Western-Blot,传输电子显微镜和免疫光学评估了ERS,亡,SO2水平和Hippo通路激活.

主要成果:

甲状腺功能障碍导致心肌纤维化,心脏功能下降,内源性SO2生成酶 (AAT1/2) 水平降低.
外源性SO2捐赠者通过上调AAT1/2.2,改善心脏功能并减少纤维化.
SO2对抗了ERS和亡,并抑制了过度的Hippo通路激活.

结论:

SO2可以改善甲状腺功能过高引起的心肌纤维化和心脏功能障碍.
SO2通过抑制Hippo路径,ERS和亡来发挥其保护作用.
二氧化是治疗HTC的潜在治疗标.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.细胞内膜网膜应激压力河马信号通道的信号通道甲状腺功能障碍症引起的心肌病.二氧化硫是二氧化硫的第二种化合物.

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