Evaluation of in vivo lithium chloride effects as a GSK3-β inhibitor on human adipose derived stem cells differentiation into oligodendrocytes and re-myelination in an animal model of multiple sclerosis

Ghosouri, Sahar; Soleimani, Mitra; Bakhtiari, M.; Ghasemi, Nazem

doi:10.1007/s11033-022-08181-8

Mol Biol Rep

2022

DOI: 10.1007/s11033-022-08181-8

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Evaluation of in vivo lithium chloride effects as a GSK3-β inhibitor on human adipose derived stem cells differentiation into oligodendrocytes and re-myelination in an animal model of multiple sclerosis

Sahar Ghosouri

Mitra Soleimani

M. Bakhtiari

et al.

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2024

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Cited by 3 publications

References 32 publications

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Therapeutic Potential Effect of Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitors in Parkinson Disease: Exploring an Overlooked Avenue

Turkistani,

Al-kuraishy,

Al-Gareeb

et al. 2024

Mol Neurobiol

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Parkinson’s disease (PD) is a progressive neurodegenerative disease of the brain due to degeneration of dopaminergic neurons in the substantia nigra (SN). Glycogen synthase kinase 3 beta (GSK-3β) is implicated in the pathogenesis of PD. Therefore, the purpose of the present review was to revise the mechanistic role of GSK-3β in PD neuropathology, and how GSK-3β inhibitors affect PD neuropathology. GSK-3 is a conserved threonine/serine kinase protein that is intricate in the regulation of cellular anabolic and catabolic pathways by modulating glycogen synthase. Over-expression of GSK-3β is also interconnected with the development of different neurodegenerative diseases. However, the underlying mechanism of GSK-3β in PD neuropathology is not fully clarified. Over-expression of GSK-3β induces the development of PD by triggering mitochondrial dysfunction and oxidative stress in the dopaminergic neurons of the SN. NF-κB and NLRP3 inflammasome are activated in response to dysregulated GSK-3β in PD leading to progressive neuronal injury. Higher expression of GSK-3β in the early stages of PD neuropathology might contribute to the reduction of neuroprotective brain-derived neurotrophic factor (BDNF). Thus, GSK-3β inhibitors may be effective in PD by reducing inflammatory and oxidative stress disorders which are associated with degeneration of dopaminergic in the SN.

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Therapeutic Potential Effect of Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitors in Parkinson Disease: Exploring an Overlooked Avenue

Turkistani,

Al-kuraishy,

Al-Gareeb

et al. 2024

Mol Neurobiol

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Adipose-derived stem cell therapy for spinal cord injuries: Advances, challenges, and future directions

Shimizu,

Ntege,

Takahara

et al. 2024

Regenerative Therapy

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Unraveling the Role of the Glycogen Synthase Kinase-3β, Bruton’s Tyrosine Kinase, and Sphingosine 1 Phosphate Pathways in Multiple Sclerosis

Mohite,

Gharat,

Doshi

2024

EMIDDT

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Inflammation, demyelination, and neurodegeneration are symptoms of the central nervous system (CNS) condition known as Multiple sclerosis (MS). Due to its crucial function in controlling immune cell activation and inflammation, the glycogen synthase kinase-3β (GSK3β), Bruton's tyrosine kinase (BTK), and Sphingosine 1 phosphate (S1P) signaling pathway have become a viable target for the therapy of MS. The GSK-3β signaling system, which controls several biological target processes, including cell survival, proliferation, and inflammation, depends on the GSK-3β enzyme. In MS animal models and human studies, GSK-3β inhibition has been demonstrated to lessen demyelination and inflammation. Clinical research on MS has demonstrated that BTK inhibitors decrease inflammation and disease activity by preventing B cell activation and the subsequent release of cytokines. Clinical investigations for MS have demonstrated that S1P modulators, such as fingolimod, lower disease activity and inflammation by limiting immune cell migration to the central nervous system and preventing cytokine production. The GSK-3β /BTK/S1P signaling pathway in MS is the subject of this paper's summary and discussion of prospective treatment targets.

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Evaluation of in vivo lithium chloride effects as a GSK3-β inhibitor on human adipose derived stem cells differentiation into oligodendrocytes and re-myelination in an animal model of multiple sclerosis

Cited by 3 publications

References 32 publications

Therapeutic Potential Effect of Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitors in Parkinson Disease: Exploring an Overlooked Avenue

Therapeutic Potential Effect of Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitors in Parkinson Disease: Exploring an Overlooked Avenue

Adipose-derived stem cell therapy for spinal cord injuries: Advances, challenges, and future directions

Unraveling the Role of the Glycogen Synthase Kinase-3β, Bruton’s Tyrosine Kinase, and Sphingosine 1 Phosphate Pathways in Multiple Sclerosis

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