Special Issue "Molecular Mechanisms and Pathophysiology of Cerebral Ischemia"
Deadline for manuscript submissions: 31 October 2021.
Interests: neurodegeneration; neurogenesis, cerebral ischemia, aging in CNS
Special Issues and Collections in MDPI journals
Cerebral ischemia is the leading cause of death worldwide. Despite great efforts to develop potential treatments, the molecular and cellular mechanisms of cerebral ischemia are not fully understood.
Many researchers have been using various animal models of cerebral ischemia with different species of animals, different methods of occlusion of blood vessels, and different periods of occlusion time. The models of cerebral ischemia can be divided into focal and global models. Focal ischemia is characterized by a reduction of cerebral blood flow in a distinct region of the brain, whereas in global ischemia, the reduction of blood flow affects the entire brain or forebrain. Neuronal or tissue damage are different according to the type of ischemic insult. In animal models of global transient cerebral or forebrain ischemia, neuronal damage/death (loss) occurs in vulnerable regions of the brain (i.e., the hippocampus), whereas in animal models of transient focal brain ischemia, neuronal loss occurs when the ischemic duration (damage) is short (mild), or infarction (necrosis) occurs when the ischemic damage (duration) is severe (long). In this regard, the mechanisms of neuronal loss or infarction are apparently different according to the type of ischemic insult.
Diverse mechanisms of pathophysiological events in ischemic damage have been suggested, including the activation of glutamate receptors, a sustained increase in intracellular calcium, oxidative stress caused by free radicals, and the activation of resident microglia related to neuroinflammatory reactions. In addition, the dysfunction of cells related to the blood–brain barrier (BBB), including endothelial cells, astrocytes and pericytes, as well as microglia, is also suggested as a possible mechanism of ischemic injuries.
This Special Issue aims to study the control or modulation of diverse pathways during or after ischemic injuries at the molecular and cellular levels to prevent, attenuate or heal ischemia damage following various brain ischemic insults.
Prof. Moo-Ho Won
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- transient or permanent ischemia
- neuronal death
- oxidative stress
- blood-brain barrier
- therapeutic strategy