FGF21型
医学
车站3
盐皮质激素受体
心力衰竭
心肌梗塞
螺内酯
肝细胞
内科学
心脏病学
SOCS3
内分泌学
STAT蛋白
GDF15型
受体
信号转导
成纤维细胞生长因子
生物
细胞生物学
体外
生物化学
作者
Jian‐Yong Sun,Lin‐Juan Du,Xuerui Shi,Yu-Yao Zhang,Yuan Liu,Yong-Li Wang,Bo‐Yan Chen,Ting Liu,Hong Zhu,Yan Liu,Chun Ruan,Zhenji Gan,Hao Ying,Zhinan Yin,Pingjin Gao,Xiaoxiang Yan,Ruo-Gu Li,Sheng‐Zhong Duan
出处
期刊:Science Advances
[American Association for the Advancement of Science (AAAS)]
日期:2023-04-05
卷期号:9 (14)
被引量:5
标识
DOI:10.1126/sciadv.ade4110
摘要
The liver plays a protective role in myocardial infarction (MI). However, very little is known about the mechanisms. Here, we identify mineralocorticoid receptor (MR) as a pivotal nexus that conveys communications between the liver and the heart during MI. Hepatocyte MR deficiency and MR antagonist spironolactone both improve cardiac repair after MI through regulation on hepatic fibroblast growth factor 21 (FGF21), illustrating an MR/FGF21 axis that underlies the liver-to-heart protection against MI. In addition, an upstreaming acute interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) pathway transmits the heart-to-liver signal to suppress MR expression after MI. Hepatocyte Il6 receptor deficiency and Stat3 deficiency both aggravate cardiac injury through their regulation on the MR/FGF21 axis. Therefore, we have unveiled an IL-6/STAT3/MR/FGF21 signaling axis that mediates heart-liver cross-talk during MI. Targeting the signaling axis and the cross-talk could provide new strategies to treat MI and heart failure.
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