PMID- 38069203
OWN - NLM
STAT- MEDLINE
DCOM- 20231216
LR  - 20231216
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 24
IP  - 23
DP  - 2023 Nov 28
TI  - Connexins Control Glial Inflammation in Various Neurological Diseases.
LID - 10.3390/ijms242316879 [doi]
LID - 16879
AB  - Connexins (Cxs) form gap junctions through homotypic/heterotypic oligomerization. 
      Cxs are initially synthesized in the endoplasmic reticulum, then assembled as 
      hexamers in the Golgi apparatus before being integrated into the cell membrane as 
      hemichannels. These hemichannels remain closed until they combine to create gap 
      junctions, directly connecting neighboring cells. Changes in the intracellular or 
      extracellular environment are believed to trigger the opening of hemichannels, 
      creating a passage between the inside and outside of the cell. The size of the 
      channel pore depends on the Cx isoform and cellular context-specific effects such 
      as posttranslational modifications. Hemichannels allow various bioactive 
      molecules, under ~1 kDa, to move in and out of the host cell in the direction of 
      the electrochemical gradient. In this review, we explore the fundamental roles of 
      Cxs and their clinical implications in various neurological dysfunctions, 
      including hereditary diseases, ischemic brain disorders, degenerative conditions, 
      demyelinating disorders, and psychiatric illnesses. The influence of Cxs on the 
      pathomechanisms of different neurological disorders varies depending on the 
      circumstances. Hemichannels are hypothesized to contribute to proinflammatory 
      effects by releasing ATP, adenosine, glutamate, and other bioactive molecules, 
      leading to neuroglial inflammation. Modulating Cxs' hemichannels has emerged as a 
      promising therapeutic approach.
FAU - Yamasaki, Ryo
AU  - Yamasaki R
AUID- ORCID: 0000-0003-2071-7861
AD  - Department of Neurology, Neurological Institute, Graduate School of Medical 
      Sciences, Kyushu University, Fukuoka 812-8582, Japan.
LA  - eng
GR  - JP 20ek019308h0003/the Japan Agency for Medical Research and Development/
GR  - JP16K09694/Japan Society for the Promotion of Science/
GR  - JP19K07963/Japan Society for the Promotion of Science/
PT  - Journal Article
PT  - Review
DEP - 20231128
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Connexins)
SB  - IM
MH  - Humans
MH  - *Connexins/metabolism
MH  - Gap Junctions/metabolism
MH  - Neuroglia/metabolism
MH  - *Nervous System Diseases/metabolism
MH  - Inflammation/metabolism
PMC - PMC10706219
OTO - NOTNLM
OT  - astroglia
OT  - autism
OT  - connexin
OT  - gap junction
OT  - hemichannel
OT  - microglia
OT  - multiple sclerosis
OT  - oligodendroglia
COIS- R.Y. has received honoraria from Ono Pharmaceutical, Takeda Pharmaceutical, 
      Eisai, Novartis, and CSL Behring.
EDAT- 2023/12/09 10:44
MHDA- 2023/12/17 09:43
PMCR- 2023/11/28
CRDT- 2023/12/09 01:15
PHST- 2023/10/07 00:00 [received]
PHST- 2023/11/25 00:00 [revised]
PHST- 2023/11/27 00:00 [accepted]
PHST- 2023/12/17 09:43 [medline]
PHST- 2023/12/09 10:44 [pubmed]
PHST- 2023/12/09 01:15 [entrez]
PHST- 2023/11/28 00:00 [pmc-release]
AID - ijms242316879 [pii]
AID - ijms-24-16879 [pii]
AID - 10.3390/ijms242316879 [doi]
PST - epublish
SO  - Int J Mol Sci. 2023 Nov 28;24(23):16879. doi: 10.3390/ijms242316879.