Molecular Research in Cerebral Ischemia: From Microglial States to Angiogenic Resilience

Dear Colleagues,

This Special Issue, "Molecular Research in Cerebral Ischemia: From Microglial States to Angiogenic Resilience", explores the dynamic cellular and molecular shifts that dictate brain recovery following ischemic insult. Traditionally viewed through the lens of acute neuronal loss, modern stroke research now recognizes the neurovascular unit (NVU) as a highly plastic ecosystem where interplay between the cerebral vasculature and the immune environment determines long-term outcomes.

This Special Issue focuses on the bidirectional signaling between the brain's innate immune system and the vascular architecture. Primary emphasis is placed on microglial plasticity, investigating how these resident immune cells transition between pro-inflammatory and pro-repair phenotypes to either exacerbate secondary injury or facilitate tissue remodeling. In parallel, this Special Issue examines the mechanisms of angiogenic resilience, highlighting how the restoration of tissue oxygenation and the formation of robust, functional microvessels can mitigate the "augmented damage" often seen in conditions such as subarachnoid hemorrhage and focal ischemia.

By bridging the gap between fundamental discovery and translational application, this Special Issue highlights innovative strategies to "reprogram" the neurovascular unit (NVU) from a mediator of injury to a driver of functional recovery. Particular emphasis is placed on the molecular and cellular mechanisms, such as microglial phenotypic switching and angiogenic resilience, that dictate the brain's capacity for self-repair.

Furthermore, this Special Issue invites investigations into how stabilizing the brain's internal environment, specifically through optimized tissue oxygenation and hemodynamic support, can interrupt the pathological cascade following hemorrhagic and/or ischemic stroke. By targeting these early physiological windows, it will identify novel interventions that halt the progression of post-stroke neurodegeneration and the transition toward chronic cognitive decline.

Dr. Abdullah Ahmad
Guest Editor

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