This review discusses the molecular pathogenesis of ischemic and hemorrhagic strokes, focusing on their underlying mechanisms and potential therapeutic approaches. Stroke is a leading cause of death and disability globally, with ischemic strokes accounting for nearly 90% of cases. Ischemic strokes result from reduced blood flow to the brain, while hemorrhagic strokes involve bleeding into the brain tissue. Both types share mechanisms such as oxidative stress, inflammation, and calcium overload, but ischemic strokes also involve excitotoxicity and neuroinflammation. The review highlights the role of non-coding RNAs, particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in stroke pathophysiology and recovery. These molecules are essential for angiogenesis and neuroprotection and have potential applications as therapeutic, diagnostic, and prognostic tools in cerebrovascular diseases. Ischemic stroke pathophysiology involves atherothrombotic processes, such as atherosclerosis and thrombosis, and embolic mechanisms, including cardiac embolism. The pathophysiology of ischemic stroke includes excitotoxicity, oxidative stress, and neuroinflammation, which contribute to neuronal damage and cell death. The review also discusses the role of cytokines such as TNF-α, IL-1β, IL-6, and IFN-γ in the inflammatory response following stroke, highlighting their dual roles in both promoting and mitigating brain damage. Neuroinflammation is a critical component of stroke pathophysiology, involving the activation of microglia and macrophages, which can lead to both pro-inflammatory and anti-inflammatory responses. The review explores the roles of various immune cells, including microglia, astrocytes, neutrophils, dendritic cells, T lymphocytes, and B cells, in the inflammatory response and tissue repair following stroke. The review also discusses the potential therapeutic strategies targeting these molecular mechanisms, including the modulation of cytokine activity, the use of non-coding RNAs, and the development of novel therapies based on molecular insights. Overall, the review emphasizes the importance of understanding the complex molecular mechanisms underlying stroke to develop effective treatments and improve patient outcomes.This review discusses the molecular pathogenesis of ischemic and hemorrhagic strokes, focusing on their underlying mechanisms and potential therapeutic approaches. Stroke is a leading cause of death and disability globally, with ischemic strokes accounting for nearly 90% of cases. Ischemic strokes result from reduced blood flow to the brain, while hemorrhagic strokes involve bleeding into the brain tissue. Both types share mechanisms such as oxidative stress, inflammation, and calcium overload, but ischemic strokes also involve excitotoxicity and neuroinflammation. The review highlights the role of non-coding RNAs, particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in stroke pathophysiology and recovery. These molecules are essential for angiogenesis and neuroprotection and have potential applications as therapeutic, diagnostic, and prognostic tools in cerebrovascular diseases. Ischemic stroke pathophysiology involves atherothrombotic processes, such as atherosclerosis and thrombosis, and embolic mechanisms, including cardiac embolism. The pathophysiology of ischemic stroke includes excitotoxicity, oxidative stress, and neuroinflammation, which contribute to neuronal damage and cell death. The review also discusses the role of cytokines such as TNF-α, IL-1β, IL-6, and IFN-γ in the inflammatory response following stroke, highlighting their dual roles in both promoting and mitigating brain damage. Neuroinflammation is a critical component of stroke pathophysiology, involving the activation of microglia and macrophages, which can lead to both pro-inflammatory and anti-inflammatory responses. The review explores the roles of various immune cells, including microglia, astrocytes, neutrophils, dendritic cells, T lymphocytes, and B cells, in the inflammatory response and tissue repair following stroke. The review also discusses the potential therapeutic strategies targeting these molecular mechanisms, including the modulation of cytokine activity, the use of non-coding RNAs, and the development of novel therapies based on molecular insights. Overall, the review emphasizes the importance of understanding the complex molecular mechanisms underlying stroke to develop effective treatments and improve patient outcomes.