Ischemic stroke is more common in the elderly, characterized by rapid onset, high incidence, high disability rate, and high mortality rate.It often causes severe cellular dysfunction and brain damage, imposing a significant burden on families and society.Death-associated protein kinase 1(DAPK1)is a calcium/calmodulin(Ca 2+ /CaM)-dependent serine/threonine(Ser/Thr)protein kinase that plays a crucial role in regulating brain damage caused by ischemic stroke.Studies have shown that DAPK1 activity is regulated by phosphorylation and mediates the pathophysiological processes of ischemic stroke through multiple signaling pathways, including DAPK1-N-methyl-D-aspartate(DAPK1-NMDA), DAPK1-NMDA), DAPK1-tumor suppressor protein p53(DAPK1-p53), DAPK1-microtubule-associated protein Tau(DAPK1-Tau), and DAPK1-dangerous signaling(DAPK1-DANGER), among others.Blocking these signaling pathways can significantly improve neuronal damage following ischemic stroke.This article reviews the related signaling pathways, mechanisms of action, and progress in targeted drug development of DAPK1 in ischemic stroke, aiming to provide references for future research and treatment of ischemic stroke.

Ischemic stroke is more common in the elderly, characterized by rapid onset, high incidence, high disability rate, and high mortality rate.It often causes severe cellular dysfunction and brain damage, imposing a significant burden on families and society.Death-associated protein kinase 1(DAPK1)is a calcium/calmodulin(Ca 2+ /CaM)-dependent serine/threonine(Ser/Thr)protein kinase that plays a crucial role in regulating brain damage caused by ischemic stroke.Studies have shown that DAPK1 activity is regulated by phosphorylation and mediates the pathophysiological processes of ischemic stroke through multiple signaling pathways, including DAPK1-N-methyl-D-aspartate(DAPK1-NMDA), DAPK1-NMDA), DAPK1-tumor suppressor protein p53(DAPK1-p53), DAPK1-microtubule-associated protein Tau(DAPK1-Tau), and DAPK1-dangerous signaling(DAPK1-DANGER), among others.Blocking these signaling pathways can significantly improve neuronal damage following ischemic stroke.This article reviews the related signaling pathways, mechanisms of action, and progress in targeted drug development of DAPK1 in ischemic stroke, aiming to provide references for future research and treatment of ischemic stroke.

Cerebral stroke has one of the highest incidence,mortality and disability rates worldwide.Al-though studies have confirmed that reperfusion therapy is an effective strategy for treating stroke patients,the secondary in-jury of brain tissue caused by reperfusion therapy,which is called cerebral ischaemia reperfusion injury(CIRI),is anoth-er medical challenge globally.The microenvironment network constructed by multicellular exosomes plays a regulatory role in the occurrence and development of CIRI.In addition,exosomes have potential value as drug delivery carriers for cerebrovascular diseases due to their stability,the ability to pass through the blood?brain barrier and other characteristics.This study reviews the research progress on the signal network constructed by multiple cells through exosomes and exo-somes as drug carriers in CIRI to provide a reference for research to improve CIRI.

The mechanism of ischemic stroke development has not been fully elucidated, but inflammatory damage has been recognized to play an important role. Activation of Toll-like receptor 4 (TLR4)-related signaling pathways can promote the expressions of pro-inflammatory cytokines and anti-inflammatory cytokines associated with ischemic stroke, thereby affecting the progression and prognosis of ischemic stroke. The author reviews the research progress of TLR4-related signaling pathways in inflammatory injury of ischemic stroke, in order to provide some ideas and references for the discovery of targeted TLR4 anti-inflammatory drugs that can be used for ischemic stroke treatment.

Ischemic stroke (IS) is one of the main causes of human death and disability all over the world. Although reperfusion treatments, such as stent implantation, cerebrovascular bypass and thrombolysis, can achieve reperfusion in ischemic regions of IS patients, cerebral ischemia-reperfusion injury (CIRI) caused by reperfusion treatment has become a difficult clinical treatment problem. At present, the clinical diagnosis and treatment methods to improve CIRI are limited and often can not obtain satisfactory effect; therefore, CIRI exploration based on molecular level to find an effective method for CIRI has become the focus of current research. Studies have confirmed that circular RNA (circRNA) participates in many physiological/pathological processes in brain CIRI and acts as an important regulator, which is expected to become a potential target for CIRI treatment. This paper focuses on the regulation of circRNA in different cerebral cellular neurons to provide new potential target for CIRI treatment and improvement.