GSK3B

Where the papers sit

22 papers from the last 6 months study GSK3B directly · updated from PubMed 12 Oct 2026

• Tissue Injury and Aging

  Inflammation, fibrosis and age-related tissue dysfunction recur across brain, heart, liver and ocular models. AKT/GSK3β inhibition or deacetylation is linked to reduced neuroinflammation, myocardial fibrosis, MASH endotheliopathy and ciliary-muscle aging. Alzheimer’s studies add pharmacophore and docking-led searches for inhibitors aimed at tauopathies. The field is moving toward tissue-specific GSK3β modulation, but diverse models and mainly in-silico or preclinical evidence leave clinical benefit unresolved.

  6 papers · 27.3%

• Cognitive Decline in Aging

  AKT/GSK3β signaling links tau hyperphosphorylation, synaptic and mitochondrial dysfunction, and neuronal apoptosis to cognitive decline. GSK3β inhibition and cistanoside A are being explored to restore cognition in Alzheimer-like models. Quercetin shifts microglial polarization through miR-379-5p in postoperative cognitive dysfunction, while obstructive sleep apnoea work seeks oxygen-related plasma biomarkers. Evidence remains preclinical or pilot-stage, leaving biomarker validation and translation open.

  4 papers · 18.2%

• Oxidative Stress in Diabetes

  Oxidative stress and apoptosis are the shared injury mechanisms in diabetic kidney and cognitive models. PI3K/Akt/GSK3β modulation is associated with lower BAX, caspase-3 and other apoptotic signals. In the diabetic brain model, the GSK3β/Nrf2 axis and antioxidant response are central, while renal work emphasizes heme oxygenase 1. The direction is toward pathway-targeted cytoprotection, but evidence remains limited to animal studies.

  2 papers · 9.1%

• Others — Mechanism-Based Drug Discovery

  Computational screening and polypharmacology recur across candidate discovery, spanning fibrosis, ischemic injury, prion toxicity, cancer, Rett syndrome and kinase inhibitor design. Network pharmacology, docking, molecular dynamics and ADMET filtering are used to prioritize mechanisms and compounds. Experimental follow-up links PI3K/AKT, PKC/XIAP and cell-cycle pathways to therapeutic response, while pharmacovigilance highlights CNS and systemic toxicity. The set has no single disease or clinical endpoint, so it is best viewed as exploratory therapeutic discovery.

  10 papers · 45.5%