Calcium/Calmodulin–Dependent Protein Kinase II in Cerebrovascular Diseases
Autor: | Jane Q Wang, Edwin S. Levitan, Xuejing Zhang, Jaclyn Connelly, Dandan Sun |
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Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Neurology Excitotoxicity Review Article medicine.disease_cause Vascular dementia 03 medical and health sciences 0302 clinical medicine Mediator Neuroinflammation Endothelial barrier dysfunction Ca2+/calmodulin-dependent protein kinase Humans Medicine cardiovascular diseases Cerebrovascular disease Stroke Neurons CaMKII business.industry musculoskeletal neural and ocular physiology General Neuroscience Glutamate receptor musculoskeletal system medicine.disease Neuronal cell death 030104 developmental biology nervous system Neuroinflammatory Diseases cardiovascular system Calcium Neurology (clinical) Calcium-Calmodulin-Dependent Protein Kinase Type 2 Cardiology and Cardiovascular Medicine business Neuroscience 030217 neurology & neurosurgery |
Zdroj: | Translational Stroke Research |
ISSN: | 1868-601X 1868-4483 |
Popis: | Cerebrovascular disease is the most common life-threatening and debilitating condition that often leads to stroke. The multifunctional calcium/calmodulin-dependent protein kinase II (CaMKII) is a key Ca2+ sensor and an important signaling protein in a variety of biological systems within the brain, heart, and vasculature. In the brain, past stroke-related studies have been mainly focused on the role of CaMKII in ischemic stroke in neurons and established CaMKII as a major mediator of neuronal cell death induced by glutamate excitotoxicity and oxidative stress following ischemic stroke. However, with growing understanding of the importance of neurovascular interactions in cerebrovascular diseases, there are clearly gaps in our understanding of how CaMKII functions in the complex neurovascular biological processes and its contributions to cerebrovascular diseases. Additionally, emerging evidence demonstrates novel regulatory mechanisms of CaMKII and potential roles of the less-studied CaMKII isoforms in the ischemic brain, which has sparked renewed interests in this dynamic kinase family. This review discusses past findings and emerging evidence on CaMKII in several major cerebrovascular dysfunctions including ischemic stroke, hemorrhagic stroke, and vascular dementia, focusing on the unique roles played by CaMKII in the underlying biological processes of neuronal cell death, neuroinflammation, and endothelial barrier dysfunction triggered by stroke. We also highlight exciting new findings, promising therapeutic agents, and future perspectives for CaMKII in cerebrovascular systems. |
Databáze: | OpenAIRE |
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