AI Article Synopsis
- Subarachnoid hemorrhage (SAH) can severely impact not only the brain but also the heart, leading to significant cardiac injuries in mice, such as extended QT intervals and reduced heart function.
- Researchers found that increased galectin-3 expression was linked to these cardiac issues and could be reversed with the galectin-3 inhibitor TD139.
- Additional findings showed that suppressing macrophage activation with propranolol improved heart function and reduced galectin-3 levels, indicating a potential therapeutic target through a macrophage-galectin-3 pathway for SAH-related cardiac problems.
Article 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.
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| http://dx.doi.org/10.1016/j.expneurol.2023.114418 | DOI Listing |
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