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Ischemic stroke is a complex and heterogeneous neurological disorder with high mortality and long-term disability rates, yet effective clinical biomarkers and targeted therapies remain elusive. Despite extensive research, the molecular mechanisms driving ischemic stroke pathophysiology are still not fully understood. Cathepsins, a family of endo/lysosomal proteases, play a crucial role in modulating neuronal protein activation and degradation, thereby exerting both neuroprotective and neurotoxic effects. This review synthesizes current findings on the neuropharmacological roles of cathepsins in ischemic stroke, highlighting their dual functions and potential as therapeutic targets. By providing an integrated perspective, this article aims to uncover novel molecular pathways implicated in stroke progression and identify innovative therapeutic strategies centered on cathepsin modulation. Furthermore, this review explores the potential of cathepsins as biomarkers, paving the way for more precise, personalized interventions that could ultimately improve patient outcomes and mitigate long-term disability in ischemic stroke survivors.
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