炎症体
生长素
糖尿病性心肌病
蛋白激酶B
串扰
上睑下垂
内科学
内分泌学
炎症
PI3K/AKT/mTOR通路
医学
心肌病
癌症研究
化学
药理学
细胞生物学
信号转导
生物
心力衰竭
受体
光学
物理
作者
Fan Wang,Jingzhi Wang,Xinfang Liang,Zixuan Wu,Jiaxin Xue,Lingyu Yin,Lai Wei,Xiaohui Zhang
标识
DOI:10.1080/1061186x.2023.2295268
摘要
AIMS: Endoplasmic reticulum stress(ERS) can induce inflammation mediated by NLRP3 inflammatory bodies and link inflammation with oxidative stress in myocardial tissue. Ghrelin is an endogenous growth hormone-releasing peptide that has been proven to have multiple effects, such as regulating energy metabolism and inhibiting inflammation. However, the role of ghrelin in myocardial injury in diabetic rats and the mechanism have not been reported. RESULTS: cardiomyocytes. Interestingly, ghrelin could activate the PI3K/AKT signalling pathway, playing a role in inhibiting endoplasmic reticulum stress and reducing the expression of pyroptosis-related proteins. However, these protective effects could be largely eliminated by LY294002. CONCLUSIONS: In summary, we demonstrated that ghrelin inhibited myocardial pyroptosis in diabetic cardiomyopathy by regulating ERS and NLRP3 inflammasome crosstalk through the PI3K/AKT pathway. Our results provide new insights into the mechanism of diabetic myocardial injury induced by high glucose and high palmitic acid and ghrelin-mediated anti-inflammatory protection and provide potential therapeutic targets and strategies for diabetic cardiomyopathy.
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