Repurposing of glatiramer acetate to treat cardiac ischemia in rodent models.
Gal AvielJacob ElkahalKfir Baruch UmanskyHanna Bueno-LevyZachary PetroverYulia KotlovskiDaria LendengoltsDavid KainTali ShalitLingling ZhangShoval MiyaraMatthias P KramerYifat MerblStav KozlovskiRonen AlonRina AharoniRuth ArnonDavid MishaliUriel KatzDean NachmanRabea AslehOffer AmirEldad TzahorRachel SarigPublished in: Nature cardiovascular research (2024)
Myocardial injury may ultimately lead to adverse ventricular remodeling and development of heart failure (HF), which is a major cause of morbidity and mortality worldwide. Given the slow pace and substantial costs of developing new therapeutics, drug repurposing is an attractive alternative. Studies of many organs, including the heart, highlight the importance of the immune system in modulating injury and repair outcomes. Glatiramer acetate (GA) is an immunomodulatory drug prescribed for patients with multiple sclerosis. Here, we report that short-term GA treatment improves cardiac function and reduces scar area in a mouse model of acute myocardial infarction and a rat model of ischemic HF. We provide mechanistic evidence indicating that, in addition to its immunomodulatory functions, GA exerts beneficial pleiotropic effects, including cardiomyocyte protection and enhanced angiogenesis. Overall, these findings highlight the potential repurposing of GA as a future therapy for a myriad of heart diseases.
Keyphrases
- pet ct
- heart failure
- left ventricular
- acute myocardial infarction
- mouse model
- acute heart failure
- atrial fibrillation
- endothelial cells
- emergency department
- wound healing
- oxidative stress
- current status
- vascular endothelial growth factor
- type diabetes
- ischemia reperfusion injury
- insulin resistance
- drug induced
- climate change
- human health
- subarachnoid hemorrhage
- catheter ablation