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GSK-3β in myocardial ischemia-reperfusion injury: molecular insights and therapeutic approaches.

Created on 02 Sep 2026

Authors

Praveena Sriharsh, Arya K Vishwapriya, Radhika Joshi, Swapnil Sharma

Published in

The Journal of pharmacy and pharmacology. Volume 78. Issue 9. Sep 01, 2026.

Abstract

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.
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.
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.
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.

PMID:
42679234
Bibliographic data and abstract were imported from PubMed on 02 Sep 2026.

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