Role of immune responses for extracellular matrix remodeling in the ischemic brain.
Egor DzyubenkoDaniel Manrique-CastanoChristoph KleinschnitzAndreas FaissnerJanine GronewoldPublished in: Therapeutic advances in neurological disorders (2018)
Neuroinflammation is one of the key components contributing to the devastating outcome of ischemic stroke. Starting with stroke onset, inflammatory processes contribute both to cell damage and tissue remodeling. The early release of alarmins triggers the upregulation of multiple proinflammatory cytokines, resulting in the compromised integrity of the blood-brain barrier. From this moment on, the infiltration of peripheral immune cells, reactive gliosis and extracellular matrix (ECM) alterations become intricately intertwined and act as one unit during the tissue remodeling. While the mechanisms of leukocyte and glia activation are amply reviewed, the field of ECM modification remains as yet under explored. In this review, we focus on the interplay between neuroinflammatory cascades and ECM in the ischemic brain. By summarizing the currently available evidence obtained by in vitro research, animal experimentation and human studies, we aim to propose a new direction for the future investigation of stroke recovery.
Keyphrases
- extracellular matrix
- cerebral ischemia
- atrial fibrillation
- subarachnoid hemorrhage
- blood brain barrier
- immune response
- brain injury
- white matter
- resting state
- endothelial cells
- single cell
- traumatic brain injury
- cell proliferation
- induced pluripotent stem cells
- poor prognosis
- current status
- functional connectivity
- cell therapy
- signaling pathway
- toll like receptor
- lipopolysaccharide induced
- multiple sclerosis
- dendritic cells
- pluripotent stem cells
- case control