Hypoxia is a key component in a number of neurological diseases. Hypoxia in pathological conditions leads to neuronal loss, glial cell activation as well as blood brain barrier (BBB) disturbance, and disruption. The activation of glial cells (both astrocyte and microglia) produces a complex array of inflammatory cytokines and are the primary focus of neuroinflammation in hypoxia and ischaemia. The aim of this research topic is to characterize both astrocyte and microglia activation in hypoxia (differing in duration and severity) and ischaemia, as well as to define the role of the hypoxia responsive (HIF; hypoxia inducible factor) and inflammatory (nuclear factor kB) transcription families and their crosstalk in neuroinflammation.
Brain cells sense and respond to hypoxia through the activity of the transcription factor, HIF, and its regulatory hydroxylases: the prolyl hydroxylase domain enzymes. In addition to their participation in endogenous neuroprotection, accumulated evidence increasingly suggests an additional important regulatory role for the HIF in neuroinflammation in hypoxia and ischaemia. As novel therapeutic agents which regulate this pathway are nearing the clinic, understanding the role of HIF in inflammation outcomes is an essential step in avoiding off-target effects and crucially, in developing new anti-inflammatory strategies.
Both microglia and astrocytes are the major immunocompetent cells of the CNS, although astrocytes are frequently overlooked in this regard. Current advances in biology enable reversible depletion of microglia with pharmacological agents. This provides an opportunity to study the role of not only microglia but also astrocyte in brain immune-response in hypoxia and ischaemia.
This Research Topic publishes the results of original research on any aspect of the scientific study of neuroinflammation in hypoxia and ischaemia. We will welcome manuscripts providing significant and interesting results contributing at advancing our knowledge of the neuroinflammation in hypoxia and ischaemia. Papers that will be deemed out of the scope of what the Editors are seeking for will be redirected to a more appropriate section of the journal. Areas to be covered in this Research Topic may include, but are not limited to:
- Neuroinflammation in different types of hypoxia (acute, chronic, intermittent)
- Timecourse of neuroinflammation responses to ischaemic stroke
- Neuroinflammation in ischaemic versus haemorrhagic stroke
- Immunomodulation as a therapy (targeting microglia, astrocytes)
- HIF activation and NFkB signalling in neuroinflamation in hypoxia and ischaemia
- Interaction between systemic inflammation and neuroinflammation in hypoxia and ischaemia
Hypoxia is a key component in a number of neurological diseases. Hypoxia in pathological conditions leads to neuronal loss, glial cell activation as well as blood brain barrier (BBB) disturbance, and disruption. The activation of glial cells (both astrocyte and microglia) produces a complex array of inflammatory cytokines and are the primary focus of neuroinflammation in hypoxia and ischaemia. The aim of this research topic is to characterize both astrocyte and microglia activation in hypoxia (differing in duration and severity) and ischaemia, as well as to define the role of the hypoxia responsive (HIF; hypoxia inducible factor) and inflammatory (nuclear factor kB) transcription families and their crosstalk in neuroinflammation.
Brain cells sense and respond to hypoxia through the activity of the transcription factor, HIF, and its regulatory hydroxylases: the prolyl hydroxylase domain enzymes. In addition to their participation in endogenous neuroprotection, accumulated evidence increasingly suggests an additional important regulatory role for the HIF in neuroinflammation in hypoxia and ischaemia. As novel therapeutic agents which regulate this pathway are nearing the clinic, understanding the role of HIF in inflammation outcomes is an essential step in avoiding off-target effects and crucially, in developing new anti-inflammatory strategies.
Both microglia and astrocytes are the major immunocompetent cells of the CNS, although astrocytes are frequently overlooked in this regard. Current advances in biology enable reversible depletion of microglia with pharmacological agents. This provides an opportunity to study the role of not only microglia but also astrocyte in brain immune-response in hypoxia and ischaemia.
This Research Topic publishes the results of original research on any aspect of the scientific study of neuroinflammation in hypoxia and ischaemia. We will welcome manuscripts providing significant and interesting results contributing at advancing our knowledge of the neuroinflammation in hypoxia and ischaemia. Papers that will be deemed out of the scope of what the Editors are seeking for will be redirected to a more appropriate section of the journal. Areas to be covered in this Research Topic may include, but are not limited to:
- Neuroinflammation in different types of hypoxia (acute, chronic, intermittent)
- Timecourse of neuroinflammation responses to ischaemic stroke
- Neuroinflammation in ischaemic versus haemorrhagic stroke
- Immunomodulation as a therapy (targeting microglia, astrocytes)
- HIF activation and NFkB signalling in neuroinflamation in hypoxia and ischaemia
- Interaction between systemic inflammation and neuroinflammation in hypoxia and ischaemia
