Irisin/PGC-1α/FNDC5 pathway in Parkinson’s disease: truth under the throes

Ali, Naif H.; Alhamdan, Nourah Ahmad; Al-kuraishy, Hayder M.; Al-Gareeb, Ali I.; Elekhnawy, Engy; Batiha, Gaber El-Saber

doi:10.1007/s00210-023-02726-9

Cited by 7 publications

(2 citation statements)

References 102 publications

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“…However, restoring the expression of FNDC5/Irisin can significantly improve the synaptic plasticity and memory function of mice 16,24 . Several studies have suggested that FNDC5/Irisin has neuroprotective effects through anti‐inflammatory and antioxidant impacts 26 . FNDC5/Irisin reduces the levels of IL‐1β, IL‐6, TNF‐α, iNOS and COX‐2 via AMPK‐NF‐κB to protect neurons of spinal cord in rats 27 .…”

Section: Discussionmentioning

confidence: 99%

“…16,24 Several studies have suggested that FNDC5/Irisin has neuroprotective effects through anti-inflammatory and antioxidant impacts. 26 FNDC5/Irisin reduces the levels of IL-1β, IL-6, TNF-α, iNOS and COX-2 via AMPK-NF-κB to protect neurons of spinal cord in rats. 27 FNDC5/Irisin decreases oxidative stress-induced neuronal damage by inhibiting the secretion of TNF-α and IL-6 through the Akt and ERK1/2.…”

Section: Fndc5 Can Significantly Inhibit Caspase3 and Bax Pathwaysmentioning

confidence: 97%

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FNDC5/Irisin protects neurons through Caspase3 and Bax pathways

Zhang,

Zhao

et al. 2024

Cell Biochemistry & Function

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Irisin is a glycosylated protein formed from the hydrolysis of fibronectin type III domain‐containing protein 5 (FNDC5). Recent studies have demonstrated that FNDC5/Irisin is involved in the regulation of glucose and lipid metabolism, it can inhibit inflammation and have neuroprotective effects. However, the effect and mechanism of FNDC5/Irisin on motor neuron‐like cell lines (NSC‐34) have not been reported. In this study, we used lipopolysaccharide to construct cellular oxidative stress injury models and investigated the potential roles of FNDC5/Irisin on neurons by different cellular and molecular pathways. Taken together, our findings showed that FNDC5/Irisin can protect neurons, and this effect might be associated with Caspase3 and Bax pathways. These results laid the foundation for neuronal protection and clinical translation of FNDC5/Irisin therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Fndc5 Can Significantly Inhibit Caspase3 and Bax Pathwaysmentioning

confidence: 97%

FNDC5/Irisin protects neurons through Caspase3 and Bax pathways

Zhang,

Zhao

et al. 2024

Cell Biochemistry & Function

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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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