Special Issue "Molecular Mechanisms and Pathophysiology of Acute Stroke 2.0"

Dear colleagues,

Stroke remains a leading cause of death and disability, and has a complex pathophysiology. Increasing evidence suggests that the brain is exquisitely sensitive to even short-duration ischemia, and that multiple mechanisms are involved in the tissue damage that results from cerebral ischemia. Ischemic stroke initiates a cascade of events, including ATP depletion, ionic dysregulation, the increased release of glutamate, the excess production of free radicals, and edema as well as inflammation; all of these events eventually contribute to cell death. In contrast, in an intracerebral hemorrhage, the oppression and destruction of brain tissue by a hematoma are the primary causes of brain injury, but the inflammation, coagulation response, and toxicity of the released hemoglobin play pivotal roles as well. Cell death after stroke has been attributed in the past mainly to necrosis or apoptosis, but recent reports show the involvement of other newly described forms of cell death.

The goal of this Special Issue is to provide a critical overview of the underlying factors involved in stroke-related brain injury, especially the role of cell signaling in excitotoxicity, inflammation, apoptosis, and the newly described types of cell death, such as ferroptosis. Gene and protein expression profiles after stroke in addition to neurogenesis, angiogenesis, and neuroplasticity are other important features in stroke, and should lead to a better understanding of the pathophysiology of acute stroke.

We warmly welcome submissions, including original articles and reviews, on these hot topics.

Dr. Adria Arboix
Dr. Teresa Gasull
Guest Editors

Manuscript Submission Information

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• stroke
• ischemic
• hemorrhagic
• neuronal death
• molecular mechanisms
• inflammation
• epigenetics
• ischemic tolerance
• ferroptosis
• free radicals