PMID- 36505409
OWN - NLM
STAT- MEDLINE
DCOM- 20221216
LR  - 20221221
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 13
DP  - 2022
TI  - Inflammation and immune cell abnormalities in intracranial aneurysm subarachnoid 
      hemorrhage (SAH): Relevant signaling pathways and therapeutic strategies.
PG  - 1027756
LID - 10.3389/fimmu.2022.1027756 [doi]
LID - 1027756
AB  - Intracranial aneurysm subarachnoid hemorrhage (SAH) is a cerebrovascular disorder 
      associated with high overall mortality. Currently, the underlying mechanisms of 
      pathological reaction after aneurysm rupture are still unclear, especially in the 
      immune microenvironment, inflammation, and relevant signaling pathways. 
      SAH-induced immune cell population alteration, immune inflammatory signaling 
      pathway activation, and active substance generation are associated with 
      pro-inflammatory cytokines, immunosuppression, and brain injury. Crosstalk 
      between immune disorders and hyperactivation of inflammatory signals aggravated 
      the devastating consequences of brain injury and cerebral vasospasm and increased 
      the risk of infection. In this review, we discussed the role of inflammation and 
      immune cell responses in the occurrence and development of aneurysm SAH, as well 
      as the most relevant immune inflammatory signaling pathways [PI3K/Akt, 
      extracellular signal-regulated kinase (ERK), hypoxia-inducible factor-1alpha 
      (HIF-1alpha), STAT, SIRT, mammalian target of rapamycin (mTOR), NLRP3, TLR4/nuclear 
      factor-kappaB (NF-kappaB), and Keap1/nuclear factor (erythroid-derived 2)-like 2 
      (Nrf2)/ARE cascades] and biomarkers in aneurysm SAH. In addition, we also 
      summarized potential therapeutic drugs targeting the aneurysm SAH immune 
      inflammatory responses, such as nimodipine, dexmedetomidine (DEX), fingolimod, 
      and genomic variation-related aneurysm prophylactic agent sunitinib. The 
      intervention of immune inflammatory responses and immune microenvironment 
      significantly reduces the secondary brain injury, thereby improving the prognosis 
      of patients admitted to SAH. Future studies should focus on exploring potential 
      immune inflammatory mechanisms and developing additional therapeutic strategies 
      for precise aneurysm SAH immune inflammatory regulation and genomic variants 
      associated with aneurysm formation.
CI  - Copyright (c) 2022 Jin, Duan, Du, Xing, Peng and Zhao.
FAU - Jin, Jing
AU  - Jin J
AD  - Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, 
      Sichuan, China.
AD  - Department of Biotherapy, Cancer Center, West China Hospital, Sichuan University, 
      Chengdu, Sichuan, China.
FAU - Duan, Jian
AU  - Duan J
AD  - Department of Cerebrovascular Disease, Suining Central Hospital, Suining, 
      Sichuan, China.
FAU - Du, Leiya
AU  - Du L
AD  - 4Department of Oncology, The Second People Hospital of Yibin, Yibin, Sichuan, 
      China.
FAU - Xing, Wenli
AU  - Xing W
AD  - Department of Cerebrovascular Disease, Suining Central Hospital, Suining, 
      Sichuan, China.
FAU - Peng, Xingchen
AU  - Peng X
AD  - Department of Biotherapy, Cancer Center, West China Hospital, Sichuan University, 
      Chengdu, Sichuan, China.
FAU - Zhao, Qijie
AU  - Zhao Q
AD  - Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, 
      Sichuan, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20221123
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 0 (Kelch-Like ECH-Associated Protein 1)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - 0 (NF-E2-Related Factor 2)
SB  - IM
MH  - Humans
MH  - *Subarachnoid Hemorrhage
MH  - Kelch-Like ECH-Associated Protein 1
MH  - *Intracranial Aneurysm
MH  - Phosphatidylinositol 3-Kinases
MH  - NF-E2-Related Factor 2
MH  - Signal Transduction
MH  - Inflammation
MH  - *Brain Injuries
PMC - PMC9727248
OTO - NOTNLM
OT  - immune cells
OT  - inflammation
OT  - signaling pathways
OT  - subarachnoid hemorrhage (SAH)
OT  - therapeutic strategies
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/12/13 06:00
MHDA- 2022/12/15 06:00
PMCR- 2022/01/01
CRDT- 2022/12/12 10:59
PHST- 2022/08/25 00:00 [received]
PHST- 2022/10/31 00:00 [accepted]
PHST- 2022/12/12 10:59 [entrez]
PHST- 2022/12/13 06:00 [pubmed]
PHST- 2022/12/15 06:00 [medline]
PHST- 2022/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2022.1027756 [doi]
PST - epublish
SO  - Front Immunol. 2022 Nov 23;13:1027756. doi: 10.3389/fimmu.2022.1027756. 
      eCollection 2022.