Mechanistic insights of neuronal death and neuroprotective therapeutic approaches in stroke

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Stroke, particularly ischemic stroke, is the leading cause of long-term disability and mortality worldwide. It occurs due to the occlusion of the cerebral arteries, which significantly reduces the delivery of blood, oxygen, and essential nutrients to brain tissues. This deprivation triggers a cascade of cellular events that ultimately leads to neuronal death. Recent studies have clarified the multifactorial pathogenesis of ischemic stroke, highlighting the roles of energy failure, excitotoxicity, oxidative stress, neuroinflammation, and apoptosis. This review aimed to provide a comprehensive insight into the fundamental mechanisms driving neuronal death triggered by ischemia and to examine the progress of neuroprotective therapeutic approaches designed to mitigate neuronal loss and promote neurological recovery after a stroke. Additionally, we explored widely accepted findings regarding the potential pathways implicated in neuronal death during ischemic stroke, including the interplay of apoptosis, autophagy, pyroptosis, ferroptosis, and necrosis, which collectively influence neuronal fate. We also discussed advancements in neuroprotective therapeutics, encompassing a range of interventions from pharmacological modulation to stem cell-based therapies, aimed at reducing neuronal injury and enhancing functional recovery following ischemic stroke. Despite these advancements, chall

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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