ReviewFrontiers in cellular neuroscience2025
Mechanistic insights into connexin-mediated neuroglia crosstalk in neurodegenerative diseases.
Review in Frontiers in cellular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Unraveling Neurodegeneration: Common Molecular Mechanisms and Novel Therapeutic Concepts in Major Neurodegenerative Disorders.Brain and behavior · 2026Review
- Connexin 50 mediates disease-relevant alpha-synuclein oligomer propagation and neuroinflammation in neurodegenerative disease.iScience · 2026Article
- Quantifying electrostatic control of docking and binding energetics in functional Cx36 gap junctions.Communications biology · 2026Article
- Connexin Regulation and Modulation of Neural Stem Cell Differentiation Induced by Cell-Permeable Itaconate.Journal of cellular physiology · 2026Article
- Physical crowding in 3D niche regulates neural stem cell differentiation via Cx43-mediated gap junction communication.iScience · 2026Article
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Effectiveness of warm acupuncture and moxibustion in the treatment of osteoarthritis: a retrospective study on clinical and molecular outcomes.Frontiers in medicine · 2026Article
- Boldo leaves reduce seizures, neuroinflammation, and hemichannel activity in a murine model of chronic epilepsy.Biological research · 2025Article
- Mitochondrial connexin 43 modulates metabolic stress adaptation in glioma cell lines.Cell communication and signaling : CCS · 2025Article
- Connexin 43 Role in Mitochondrial Transfer and Homeostasis in the Central Nervous System.Journal of cellular physiology · 2025Review
- Glial connexins in glaucoma.Frontiers in neuroscience · 2025Review
Corrections and comments
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Authors and funding
4 authors.
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Abstract
Neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Multiple Sclerosis (MS), and Huntington's disease (HD), although distinct in their clinical manifestations, share a common hallmark: a disrupted neuroinflammatory environment orchestrated by dysregulation of neuroglial intercellular communication. Neuroglial crosstalk is physiologically ensured by extracellular mediators and by the activity of connexins (Cxs), the forming proteins of gap junctions (Gjs) and hemichannels (HCs), which maintain intracellular and extracellular homeostasis. However, accumulating evidence suggests that Cxs can also act as pathological pore in neuroinflammatory conditions, thereby contributing to neurodegenerative phenomena such as synaptic dysfunction, oxidative stress, and ultimately cell death. This review explores mechanistic insights of Cxs-mediated intercellular communication in the progression of neurodegenerative diseases and discusses the therapeutic potential of targeting Cxs to restore cellular homeostasis.
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Registered trials
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