About this Research Topic
Brain ischemia may result from ischemic stroke or cardiac arrest, and the insufficient blood flow to the brain leads to severe brain tissue damage. Brain ischemia is one of the leading causes of death and long-term neurological disability. Treatments remain limited for rescuing brain tissue loss and promoting functional recovery.
The blood-brain barrier (BBB) maintains brain homeostasis by regulating the balance of molecules, ions, and cells between the blood and the brain. BBB disruption is one of the critical pathologies in ischemic brain injury; the severity of BBB disruption predicts neurological deficits. Focusing treatment on protecting BBB integrity can reduce neuronal injury, decrease brain edema, attenuate hemorrhagic transformation, and improve neurological outcomes. Targeting BBB disruption is thus a promising strategy for brain ischemia intervention. Emerging studies are dedicated to understanding the underlying cellular and molecular mechanisms of BBB disruption, developing new diagnostic tools, and finding therapeutic strategies targeting BBB disruption after brain ischemia.
The mechanisms of BBB disruption during brain ischemia include disruption of tight junction proteins and the extracellular matrix, and dysfunction of the transporters (such as ABC transporters, solute carriers, and aquaporins). In addition, multiple cell types such as perivascular cells and perivascular immune cells play dynamic roles in maintaining or disturbing BBB integrity and cerebral autoregulation. Emerging studies also highlighted the cellular and molecular changes in BBB integrity and cerebral angiogenesis during the chronic phase after brain ischemia. Important questions remain to be addressed about persisting BBB permeability accompanying incomplete neurological recovery and secondary neurodegeneration. A better understanding of BBB disruption and restoration will eventually contribute to preventing or reducing brain tissue damage, improving functional recovery and brain repair. Also of note is the fact that at present, the only available effective treatments for ischemic stroke are thrombectomy and tissue plasminogen activators (t-PA), treatments that can cause BBB disruption and hemorrhagic transformation. Experimental and clinical studies are needed to identify means of alleviating BBB disruption and maximizing the therapeutic effects of these treatments.
This Research Topic aims to provide a comprehensive overview of recent progress in our understanding of the cellular and molecular biology of BBB disruption in brain ischemia and novel therapeutic strategies targeting the BBB for brain recovery. We welcome the submission of original research contributions and reviews covering, but not limited to, the following topics:
1. The cellular and molecular mechanisms underlying BBB disruption induced by brain ischemia.
2. Experimental and clinical studies for neuroprotection and brain remodeling by targeting BBB injury after brain ischemia.
3. The application of traditional and novel methods and technologies for studying BBB disruption after brain ischemia.
4. Thrombolysis and thrombectomy-induced BBB disruption and hemorrhagic transformation.
The blood-brain barrier (BBB) maintains brain homeostasis by regulating the balance of molecules, ions, and cells between the blood and the brain. BBB disruption is one of the critical pathologies in ischemic brain injury; the severity of BBB disruption predicts neurological deficits. Focusing treatment on protecting BBB integrity can reduce neuronal injury, decrease brain edema, attenuate hemorrhagic transformation, and improve neurological outcomes. Targeting BBB disruption is thus a promising strategy for brain ischemia intervention. Emerging studies are dedicated to understanding the underlying cellular and molecular mechanisms of BBB disruption, developing new diagnostic tools, and finding therapeutic strategies targeting BBB disruption after brain ischemia.
The mechanisms of BBB disruption during brain ischemia include disruption of tight junction proteins and the extracellular matrix, and dysfunction of the transporters (such as ABC transporters, solute carriers, and aquaporins). In addition, multiple cell types such as perivascular cells and perivascular immune cells play dynamic roles in maintaining or disturbing BBB integrity and cerebral autoregulation. Emerging studies also highlighted the cellular and molecular changes in BBB integrity and cerebral angiogenesis during the chronic phase after brain ischemia. Important questions remain to be addressed about persisting BBB permeability accompanying incomplete neurological recovery and secondary neurodegeneration. A better understanding of BBB disruption and restoration will eventually contribute to preventing or reducing brain tissue damage, improving functional recovery and brain repair. Also of note is the fact that at present, the only available effective treatments for ischemic stroke are thrombectomy and tissue plasminogen activators (t-PA), treatments that can cause BBB disruption and hemorrhagic transformation. Experimental and clinical studies are needed to identify means of alleviating BBB disruption and maximizing the therapeutic effects of these treatments.
This Research Topic aims to provide a comprehensive overview of recent progress in our understanding of the cellular and molecular biology of BBB disruption in brain ischemia and novel therapeutic strategies targeting the BBB for brain recovery. We welcome the submission of original research contributions and reviews covering, but not limited to, the following topics:
1. The cellular and molecular mechanisms underlying BBB disruption induced by brain ischemia.
2. Experimental and clinical studies for neuroprotection and brain remodeling by targeting BBB injury after brain ischemia.
3. The application of traditional and novel methods and technologies for studying BBB disruption after brain ischemia.
4. Thrombolysis and thrombectomy-induced BBB disruption and hemorrhagic transformation.
Keywords: Brain ischemia, Blood-brain-barrier disruption, Hemorrhagic transformation, Cellular and molecular mechanisms, Neuroprotection and brain remodeling
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
