The Role of Mitochondrial Biogenesis in Ischemic Stroke

Abstract

Ischaemic stroke is a sudden neurological disorder caused by localised cerebral ischaemia and persistent cerebral infarction. Occlusion of large arteries due to atherothrombosis, cerebral embolism (i.e., embolic infarction), no thrombotic occlusion in small, deep cerebral arteries (i.e., lacunar infarction), and stenosis of proximal arteries due to hypotension leading to decreased cerebral blood flow in arterial supply zones are the most common causes of ischemic stroke (i.e., hemodynamic stroke). It is now known that organelles play an important role in various signaling events and cellular functions. The molecular mechanisms of mitochondria are involved in cerebral ischemia by generating and scavenging reactive oxygen species, apoptosis, biogenesis, mitochondrial dynamics, and inflammation are all examples of electron transport chain dysfunction. More knowledge about the involvement of mitochondria in ischemia-induced neuronal death and neuronal protection will contribute to the development of better treatment programs for stroke syndromes such as ischemic stroke.

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

“…tPA can improve cerebral blood flow and alleviate brain tissue damage, but it can increase the risk of hemorrhagic transformation and cerebral edema ( Shah, Paul & Yadav, 2024 ). Only about 8% of patients with IS are eligible for tPA ( Shademan et al, 2023 ). A previous study confirmed that cerebral apoplexy can induce reactive angiogenesis in ischemic areas ( Hatakeyama, Ninomiya & Kanazawa, 2020 ).…”