Delayed CO 2 postconditioning promotes neurological recovery after cryogenic traumatic brain injury by downregulating IRF7 expression.
Yan LiRu ChenGui-Ping ShenJing YinYu LiJing ZhaoFang NanShu-Han ZhangHui-Feng ZhangCai-Hong YangMei-Na WuYan-Ying FanPublished in: CNS neuroscience & therapeutics (2023)
We first showed that DCPC promoted functional recovery and brain tissue repair, which opens a new therapeutic time window of postconditioning for TBI. Inhibition of IRF7 is a key molecular mechanism for the beneficial effects of DCPC, and IRF7 may be a potential therapeutic target for rehabilitation after TBI.
Keyphrases
- cerebral ischemia
- traumatic brain injury
- dendritic cells
- resting state
- subarachnoid hemorrhage
- ischemia reperfusion injury
- white matter
- poor prognosis
- blood brain barrier
- brain injury
- spinal cord injury
- severe traumatic brain injury
- functional connectivity
- mild traumatic brain injury
- human health
- multiple sclerosis
- risk assessment
- climate change
- oxidative stress
- immune response