1. Academic Validation
  2. Role of galectin-3 in cardiac dysfunction induced by subarachnoid hemorrhage

Role of galectin-3 in cardiac dysfunction induced by subarachnoid hemorrhage

  • Exp Neurol. 2023 Apr 19;114418. doi: 10.1016/j.expneurol.2023.114418.
Xuan-Xuan Huang 1 Qian-Qian Zhang 1 Xiang-Xiong Pang 1 Hong-Bin Lin 1 Wan-Ying He 1 Dan Yuan 1 Wen-Jing Guo 1 Hong-Fei Zhang 2 Feng-Xian Li 3
Affiliations

Affiliations

  • 1 Department of Anesthesiology, Zhujiang Hospital of Southern Medical University, Guangzhou 510282, China.
  • 2 Department of Anesthesiology, Zhujiang Hospital of Southern Medical University, Guangzhou 510282, China. Electronic address: zhanghongfei@smu.edu.cn.
  • 3 Department of Anesthesiology, Zhujiang Hospital of Southern Medical University, Guangzhou 510282, China. Electronic address: lifengxian81@smu.edu.cn.
Abstract

Subarachnoid hemorrhage (SAH) is a severe acute cerebrovascular event that not only impairs the central nervous system but also negatively affects various other organs, including the heart. The underlying mechanisms, however, remain unclear. In this study, we discovered that mice with SAH exhibited significant cardiac injuries, such as extended QT and QTc intervals, cardiac fibrosis, and reduced cardiac ejection fractions. This phenomenon was accompanied by increased Galectin-3 expression in the cardiac ventricle and can be reversed by Galectin-3 Inhibitor TD139. Interestingly, we also observed increased co-expression of Galectin-3 in macrophage within the heart tissue of SAH mice. Additionally, when macrophage activation was suppressed using the beta-blocker propranolol, cardiac function improved, and Galectin-3 expression in the cardiac tissue decreased. Collectively, our findings offer new insights into the role of Galectin-3 in SAH-related cardiac dysfunction and suggest a macrophage-galectin-3 axis as a potential therapeutic strategy.

Keywords

Cardiac dysfunction; Galectin-3; Macrophage; Subarachnoid hemorrhage.

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