Stroke is the second cause of death globally and the third cause of global disability, causing substantial health and socioeconomic problems. Clinically, Stroke is defined as brain tissue injury caused by a lack of blood supply to a particular area, resulting in permanent nerve damage or death. Stroke is also frequently associated with metabolic causes, including insulin resistance, obesity, hypertension, and type 2 diabetes mellitus (T2DM), significantly influencing the composition and abundance of the gut microbiota. Therefore, identifying potential risk factors influencing stroke prognosis and underlying pathogenic mechanisms is essential for better management and treatment of Stroke. Several studies show the existence of two-way communication between the gut and the brain through the gut microbiota. Intimate two-way interactions between the gut and the brain occur via neural (central, autonomic, and enteric nervous systems), hormonal (endocrine system), and immunological (innate and acquired immune systems) pathways, commonly referred to as the gut-microbiota axis. Brain or gut-brain axis (Gut-Brain Axis/GBA). Gut microbiota and derived metabolites play an important role in brain function by regulating GBA signaling. Recent evidence also suggests that GBA is critical in regulating immune function post-stroke. Intestinal dysbiosis provides a chronic peripheral and central inflammatory response that accelerates stroke pathology. Gut microbial dysbiosis is a significant risk factor positively correlated with poor post-stroke outcomes. This literature review summarizes the pathogenesis of ischemic Stroke, the description of the gut microbiota, and preclinical and clinical evidence indicating the pathogenic influence of gut dysbiosis in cerebral ischemic Stroke. Keywords: Stroke, Gut-brain axis, dysbiosis
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