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

Area of Science:

• Cardiovascular Medicine
• Neuroscience
• Immunology

Background:

• Subarachnoid hemorrhage (SAH) is a critical cerebrovascular event with systemic complications.
• SAH adversely affects cardiac function, but the underlying mechanisms remain poorly understood.
• Cardiac dysfunction following SAH poses significant risks to patient outcomes.

Purpose of the Study:

• To elucidate the mechanisms of cardiac injury in the context of SAH.
• To investigate the role of galectin-3 and cardiac macrophages in SAH-induced cardiac dysfunction.
• To explore potential therapeutic targets for mitigating SAH-related cardiac complications.

Main Methods:

• SAH was induced in a mouse model to assess cardiac function and histology.
• Cardiac injury markers, including QT/QTc intervals, ejection fraction, and fibrosis, were evaluated.
• Galectin-3 expression in cardiac tissue and its co-localization with macrophages were analyzed.
• The effects of galectin-3 inhibition (TD139) and macrophage suppression (propranolol) were examined.

Main Results:

• SAH mice displayed significant cardiac injuries: prolonged QT/QTc intervals, fibrosis, and reduced ejection fraction.
• Increased cardiac galectin-3 expression, particularly within macrophages, was observed in SAH mice.
• Treatment with galectin-3 inhibitor TD139 reversed cardiac dysfunction.
• Suppression of macrophage activation with propranolol improved cardiac function and reduced galectin-3 levels.

Conclusions:

• Galectin-3 plays a critical role in the pathogenesis of cardiac dysfunction following SAH.
• A macrophage-galectin-3 axis is implicated in SAH-induced cardiac injury.
• Targeting galectin-3 or macrophage activation presents a promising therapeutic strategy for SAH-related cardiac complications.