Bridging Stroke Pathophysiology and Therapy: A Translational Perspective ^†

Stroke is a major neurological disorder and remains one of the leading causes of death and long-term disability globally [1,2,3,4]. Its pathophysiology is highly complex, necessitating a deeper understanding to support the development of more effective and safer therapeutic strategies [4]. Despite the advances in acute care, currently available therapies are limited by narrow therapeutic windows and significant side effects [2,4]. In this context, the present study focuses on two primary objectives: (i) the identification of key risk factors contributing to stroke onset—including patient-specific elements (e.g., genetic predisposition), therapeutic factors (e.g., drug–drug and food–drug interactions), and lifestyle influences—and (ii) the investigation of core molecular mechanisms involved in stroke pathogenesis. Particular emphasis is placed on inflammation, oxidative stress, endothelial dysfunction, and hemodynamic imbalance [3]. These mechanisms are examined in the context of both established treatments and emerging therapeutic strategies, including neuroprotective agents, personalized medicine, and gene therapy. By integrating mechanistic insights with translational therapeutic approaches, this work aims to contribute to the identification of novel avenues for stroke prevention (e.g., natural agents) and intervention [5]. The findings highlight the importance of interdisciplinary research in bridging the gap between fundamental science and clinical application in stroke management.