GSK-3β in myocardial ischemia-reperfusion injury: molecular insights and therapeutic approaches.
P, S., AK, V., R, J., & S, S. (2026). GSK-3β in myocardial ischemia-reperfusion injury: molecular insights and therapeutic approaches.. The Journal of pharmacy and pharmacology. https://doi.org/10.1093/jpp/rgag095
P S, AK V, R J, S S. GSK-3β in myocardial ischemia-reperfusion injury: molecular insights and therapeutic approaches.. The Journal of pharmacy and pharmacology. 2026; doi: 10.1093/jpp/rgag095
P S, AK V, R J, et al. GSK-3β in myocardial ischemia-reperfusion injury: molecular insights and therapeutic approaches.[J]. The Journal of pharmacy and pharmacology. 2026. DOI: 10.1093/jpp/rgag095.
@article{p2026,
author = {Sriharsh P and Vishwapriya AK and Joshi R and Sharma S},
title = {GSK-3β in myocardial ischemia-reperfusion injury: molecular insights and therapeutic approaches.},
journal = {The Journal of pharmacy and pharmacology},
year = {2026},
doi = {10.1093/jpp/rgag095},
note = {PMID: 42679234},
}
TY - JOUR AU - Sriharsh P AU - Vishwapriya AK AU - Joshi R AU - Sharma S TI - GSK-3β in myocardial ischemia-reperfusion injury: molecular insights and therapeutic approaches. T2 - The Journal of pharmacy and pharmacology PY - 2026 DO - 10.1093/jpp/rgag095 AN - PMID:42679234 ER -
OBJECTIVES: To synthesize current evidence on the role of glycogen synthase kinase-3β (GSK-3β) in myocardial ischemia-reperfusion injury (MIRI) and evaluate its potential as a therapeutic target. METHODS: This review examines the mechanistic involvement of GSK-3β in MIRI, focusing on mitochondrial permeability transition pore opening, apoptosis, inflammation, autophagy, and associated signaling pathways. Recent pharmacological advances in GSK-3β inhibition and their translational potential were also evaluated. KEY FINDINGS: GSK-3β is a central regulator of the pathophysiological response to MIRI. Its temporal inactivation during reperfusion confers cardioprotection through pathways including PI3K/Akt and mTOR, whereas context-dependent activation may exacerbate myocardial injury. Recent GSK-3β inhibitors show therapeutic promise, although challenges including isoform selectivity and systemic toxicity remain. CONCLUSIONS: GSK-3β represents a complex yet promising therapeutic target in ischemic heart disease. Future research should prioritize precision therapies and biomarker-guided interventions to improve the clinical translation of GSK-3β-targeted strategies.