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IL6/阿迪波涅丁/HMGB1反循环介导脂肪细胞和巨细胞交叉和心肌梗塞后的M2极化

Yue Zheng^1,2,3, Yuchao Wang^1,2,3, Bingcai Qi^2,3,4

¹School of Medicine, Nankai University, Tianjin, China.

Frontiers in immunology

|April 11, 2024

概括

这项研究揭示了心脏边界区域的IL6/ADPN/HMGB1轴,这对心脏病发作后的结果至关重要. 针对这个循环可能为心脏修复和减少衰老提供新的治疗方法.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
再生医学是一种再生医学.

背景情况:

左心室动脉瘤 (LVA) 和心肌梗塞 (MI) 有不同的后发作结果.
低值开发和边境区机制仍未得到充分研究.
了解这些差异对于治疗策略至关重要.

研究的目的:

调查LVA和MI之间的边境区的差异.
为了阐明底层的分子机制.
为了确定潜在的治疗目标,对心脏病发作后的并发症.

主要方法:

开发一种新的LVA小鼠模型.
心脏边界区域的回声心脏学,组织学和RNA测序.
在体外和体内对氨酸 (ADPN) 和其在巨细胞中的作用的研究,使用qPCR,西斑,TEM和ChIP测试.
在人类脂肪组织和血液样本中进行验证.

主要成果:

与心脏病发作相比,LVA模型显示心脏功能降低.
亚迪波涅丁 (ADPN) 通过ADPN/AdipoR2/HMGB1轴减少了,促进了淋巴血管生成,并通过ADPN/AdipoR2/HMGB1轴维持了线粒体质量.
确定了IL6/ADPN/HMGB1轴,涉及脂肪细胞和巨细胞之间的通信,影响心肌损伤.
脂肪细胞中的STAT3激活促进了ADPN表达,影响了淋巴血管生成和心肌损伤.

结论:

在心脏边界区域的IL6/ADPN/HMGB1循环决定了心脏病发作后的结果.
针对这一轴,为心脏淋巴调节和减少衰老提供了一个新的治疗策略.
这个轴可以作为超重的MI患者接受CABG的生物标志物.

关键词:

在IL6 IL6 IL6 IL6 IL6 在LNP-MertKK中.没有任何的Adiponectin.淋巴细胞血管生成巨细胞是一个巨细胞.心肌梗塞的心脏病发作

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