Abstract
Neurological deficits and cognitive dysfunctions caused by acute ischemic stroke pose enormous burden to the stroke families and the communities. Restoration of the normal function of the neurovascular unit following ischemic stroke is critical for improving neurological recovery and cognitive functions after stroke. Recent evidence suggests that the myeloid cells including both the resident microglia and infiltrating monocytes/macrophages and neutrophils are highly plastic in response to the environmental cues. They intimately interact with multiple components of the neurovascular unit in response to the alarmins, danger associated pattern molecules (DAMPs) and other signals released from the ischemic brain. The aim of this review is to discuss the reciprocal interactions between the myeloid cells and the ischemic neurovascular unit during the late repair phase of cerebral ischemic stroke. We also summarize potential immunotherapeutic targets on myeloid cells and new therapeutic approaches targeting myeloid cells, such as cell transplantation, mitochondrial dynamic and extracellular vesicles-based therapy et al to enhance neurovascular repair for better stroke recovery.
Highlights
The neurovascular unit (NVU) is composed by neurons, endothelial cells, pericytes, smooth muscle cells, astrocytes, microglia and extracellular matrix components
We summarize potential immunotherapeutic targets on myeloid cells and new therapeutic approaches targeting myeloid cells, such as cell transplantation, mitochondrial dynamic and extracellular vesicles-based therapy et al to enhance neurovascular repair for better stroke recovery
In response to cerebral ischemic stroke, the integrity of the blood brain barrier (BBB) compromises leading to leakage of harmful blood components into the central nervous system (CNS), immune cell infiltration, and aberrant transport and clearance of molecules
Summary
The neurovascular unit (NVU) is composed by neurons, endothelial cells, pericytes, smooth muscle cells, astrocytes, microglia and extracellular matrix components. It maintains brain homeostasis of the brain (Banks et al, 2018; Morrison and Filosa, 2019). In response to cerebral ischemic stroke, the integrity of the BBB compromises leading to leakage of harmful blood components into the CNS, immune cell infiltration, and aberrant transport and clearance of molecules All these changes contribute to the dysfunction of the NVU which is associated with long term neurological impairments (Fisher and Saver, 2015; Villaseñor et al, 2017).
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