Brown adipose tissue activation promotes antiapoptotic and neuroprotective effects postcerebral ischemia via increasing 14-3-3zeta secretion from circulating extracellular vesicles

Stroke has been noted as the 2nd leading cause of death worldwide, as well as the 3rd largest contributor to disability-adjusted life-years, a measure of overall disease burden in a population (1). Out of all of the new stroke cases in 2019, ischemic stroke (IS) accounted for 62.4% of them, which has led to the preservation of the ischemic penumbra to become a critical therapeutic target during the acute phase of IS. Current strategies to preserve that penumbral tissue focus on reperfusion therapy and cerebral cyto-protection, of which for the former, significant advances in recent years have been made; however, for the latter, neuroprotective agents, with proven clinical efficiency, have not been specifically identified .Brown adipose tissue (BAT) possesses both thermogenic and endocrine functions, leading to it being considered as a potential therapeutic target for various diseases; however, its role in cerebrovascular pathologies is still largely unknown. Here, we aimed to elucidate BAT activation impacts on cerebral ischemic stroke and their underlying mechanisms, using in vivo, in vitro, and acute ischemic stroke (AIS) patient analyses.This study aims to provide clarity for this matter, mainly via examining the effects of intraperitoneal BAT transplantation into a middle cerebral artery occlusion (MCAO) mouse model, where it was found that BAT transplantation was associated with lowered infarct sizes and improved neuronal function.