Ischemic stroke occurs when the arteries supplying blood to the brain are narrowed or blocked, inducing damage to brain tissue due to a lack of blood supply. One effective way to reduce brain damage and alleviate symptoms is to reopen blocked blood vessels in a timely manner and reduce neuronal damage. To achieve this, researchers have focused on identifying key cellular signaling pathways that can be targeted with drugs. These pathways include oxidative/nitrosative stress, excitatory amino acids and their receptors, inflammatory signaling molecules, metabolic pathways, ion channels, and other molecular events involved in stroke pathology. However, evidence suggests that solely focusing on protecting neurons may not yield satisfactory clinical results. Instead, researchers should consider the multifactorial and complex mechanisms underlying stroke pathology, including the interactions between different components of the neurovascular unit. Such an approach is more representative of the actual pathological process observed in clinical settings. This review summarizes recent research on the multiple molecular mechanisms and drug targets in ischemic stroke, as well as recent advances in novel therapeutic strategies. Finally, we discuss the challenges and future prospects of new strategies based on the biological characteristics of stroke.

当向大脑供血的动脉变窄或阻塞，导致脑组织因血液供应不足而受损时，就会发生缺血性中风。减少脑损伤、缓解症状的有效方法之一是及时重新开通阻塞的血管，减少神经元损伤。为了实现这一目标，研究人员专注于确定可以用药物靶向的关键细胞信号传导途径。这些途径包括氧化/亚硝化应激、兴奋性氨基酸及其受体、炎症信号分子、代谢途径、离子通道和中风病理学中涉及的其他分子事件。然而，有证据表明，仅仅关注保护神经元可能不会产生令人满意的临床结果。相反，研究人员应该考虑中风病理学背后的多因素和复杂机制，包括神经血管单元不同组成部分之间的相互作用。这种方法更能代表临床环境中观察到的实际病理过程。本文综述了缺血性脑卒中多分子机制和药物靶点的最新研究，以及新型治疗策略的最新进展。最后，我们讨论了基于卒中生物学特征的新策略的挑战和未来前景。