- VernacularTitle:Cx43及其蛋白修饰对神经炎症的调控效应:抑郁症发病机制的潜在研究靶点
- Author:
Xuan ZENG
1
;
Zi-han YAN
;
Zhi-feng TIAN
;
Hong-bin WANG
;
Qi-di AI
;
Mei-yu LIN
;
Xuan LIU
;
Nai-hong CHEN
;
Song-wei YANG
;
Yan-tao YANG
Author Information
- Publication Type:Journal Article
- Keywords: depression; gap junction; connexin 43; phospho-rylation; ubiquitination; neuroinflammation
- From: Chinese Pharmacological Bulletin 2025;41(11):2027-2031
- CountryChina
- Language:Chinese
- Abstract: Numerous studies have shown that depression is main-ly associated with the abnormal expression of connexin 43(Cx43)in astrocytes(Astro)and its mediated dysfunction of gap junction(GJ).However,the molecular mechanism of post-translational modifications targeting Cx43 to regulate neuroin-flammation-associated depression is still unclear.Post-transla-tional modifications of Cx43 mainly include phosphorylation of specific amino acid sites by PKC,PKA,PKG,MAPK and PTK,and protein degradation of Cx43 through the K48/K63 polyubiq-uitylation and deubiquitination pathways,which ultimately lead to protein degradation through K48/K63 polyubiquitination and deubiquitination.These modifications are ultimately involved in the regulation of neuroinflammatory responses through the associ-ation of GJ function.In this paper,we systematically review the role of Cx43 post-translational modifications in neuroinflamma-tion,with the aim of further exploring the potential application of targeting these modifications to modulate the inflammatory re-sponse mechanism in improving depressive symptoms.

