ArticleCell communication and signaling : CCS2025
Mitochondrial connexin 43 modulates metabolic stress adaptation in glioma cell lines.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Engineered Tan-CDs@AS-IV Nanosystem Orchestrates Mitochondrial Biogenesis and Intercellular Transfer to Restore Endothelial Function via PGC-1α and Cx43 Signaling Pathways.Nanomaterials (Basel, Switzerland) · 2026Article
- Multiscale Mechanisms of Exercise-Induced Neuroplasticity: From Molecular Pathways to Network Dynamics and Behavioral Adaptation.Brain sciences · 2026Review
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11 authors.
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Abstract
backgroundConnexin 43 (CX43) is a hemichannel (HC)- and gap junction (GJ)-forming protein that mediates the exchange of small molecules between the intracellular and extracellular environments, as well as intercellular communication. In addition to this canonical role, recent studies have shown that its functions range from transcriptional regulation to intracellular homeostasis. The ability of CX43 to translocate into mitochondria suggests its involvement in energy metabolism. However, the functions of mitochondrial CX43 (mt-CX43) in neural cells remain unexplored.
methodsOur study investigated the expression and localisation of mt-CX43 through western blot and immunofluorescence analyses in four immortalised human glioma cell lines: T98-G, A-172, CCF-STTG1, and U-87 MG. Additionally, targeted metabolomic analysis was conducted to assess changes in key metabolic pathways.
resultsBasal CX43 expression and extracellular stress factors, particularly cell density and extracellular pH fluctuations, significantly modulated the mitochondrial localisation of CX43. Inhibition of the heat shock protein 90 (HSP90) chaperone system by geldanamycin (GA) resulted in a marked reduction in mt-CX43, suggesting an import mechanism involving HSP90 and the translocase of the outer membrane (TOM) complex. In addition, the assessment of key metabolites revealed increased purine biosynthesis in T98-G cells exposed to GA treatment, characterised by lower basal CX43 expression and reduced mt-CX43 levels under stress conditions. Conversely, U-87 MG cells exhibited a stable NAD
conclusionsOur results suggest that mt-CX43 serves as a multifunctional regulator of metabolic adaptation and stress response in glioma cell lines. Our results extend the role of mt-CX43 as an essential factor in cellular metabolic plasticity, providing new insights into the modulation of metabolic imbalances and mitochondrial dysfunction.
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