Targeting autophagy, oxidative stress, and ER stress for neurodegenerative disease treatment

Esmaeili, Yasaman; Yarjanli, Zahra; Pakniya, Fatemeh; Bidram, Elham; Łos, Marek; Eshraghi, Mehdi; Klionsky, Daniel J.; Ghavami, Saeid; Zarrabi, Ali

doi:10.1016/j.jconrel.2022.03.001

Cited by 73 publications

(46 citation statements)

References 360 publications

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“…Autophagy, as a highly conserved lysosomal degradation and clearance pathway, is required for proper proliferation/migration, differentiation, development, remodeling, and intracellular refreshment [ [59] , [60] , [61] ]. An autophagosome marker, namely microtubule-associated protein light chain 3 beta (LC3β) contributes to the generation or degradation of autophagosomes [ [62] , [63] , [64] ].…”

Section: Resultsmentioning

confidence: 99%

Potential role of TGFΒ and autophagy in early cerebellum development

Dalvand¹,

Rosa²,

Ghavami³

et al. 2022

Biochemistry and Biophysics Reports

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Section: Resultsmentioning

confidence: 99%

Potential role of TGFΒ and autophagy in early cerebellum development

Dalvand¹,

Rosa²,

Ghavami³

et al. 2022

Biochemistry and Biophysics Reports

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“…AMPK promotes autophagy through phosphorylation of ULK1 [41]. AMPK also phosphorylates Beclin1, a multi-domain protein that forms a complex essential for increase of autophagosome formation [42][43][44][45]. In contrast, mTOR activation suppresses autophagy activity by preventing ULK1 and disrupting interaction between ULK1 and AMPK.…”

Section: Discussionmentioning

confidence: 99%

Methanolic Extract of Boswellia serrata Gum Protects the Nigral Dopaminergic Neurons from Rotenone-Induced Neurotoxicity

et al. 2022

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Boswellia serrata gum is a natural product that showed beneficial effects on neurodegenerative diseases in recent studies. In this study, we investigated the effects of Boswellia serrata resin on rotenone-induced dopaminergic neurotoxicity. Firstly, we attempted to see if the resin can induce AMP-activated protein kinase (AMPK) signaling pathway which has been known to have broad neuroprotective effects. Boswellia increased AMPK phosphorylation and reduced phosphorylation of mammalian target of rapamycin (p-mTOR) and α-synuclein (p-α-synuclein) in the striatum while increased the expression level of Beclin1, a marker for autophagy and brain-derived neurotrophic factor. Next, we examined the neuroprotective effects of the Boswellia extract in the rotenone-injected mice. The results showed that Boswellia evidently attenuated the loss of the nigrostriatal dopaminergic neurons and microglial activation caused by rotenone. Moreover, Boswellia ameliorated rotenone-induced decrease in the striatal dopamine and impairment in motor function. Accumulation of α-synuclein meditated by rotenone was significantly ameliorated by Boswellia. Also, we showed that β-boswellic acid, the active constituents of Boswellia serrata gum, induced AMPK phosphorylation and attenuated α-synuclein phosphorylation in SHSY5 cells. These results suggest that Boswellia protected the dopaminergic neurons from rotenone neurotoxicity via activation of the AMPK pathway which might be associated with attenuation of α-synuclein aggregation and neuroinflammation. Further investigations are warranted to identify specific molecules in Boswellia which are responsible for the neuroprotection.

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“…Therefore, we examined the effect of PDGF on autophagy-mediated pyroptosis signaling pathways after TBI, and the results were similar to the PDGF on ER stress-mediated pyroptosis. Prior studies have demonstrated that there are complex interaction between autophagy and ER stress in the neurodegenerative disease ( Esmaeili et al, 2022 ). Numerous studies reported that ER stress triggers autophagy after SCI ( Zhou et al, 2017 ; Wang et al, 2018 ; Bisicchia et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Platelet derived growth factor promotes the recovery of traumatic brain injury by inhibiting endoplasmic reticulum stress and autophagy-mediated pyroptosis

Zhang²,

Meng³

et al. 2022

Front. Pharmacol.

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Autophagy and endoplasmic reticulum stress (ER stress) are important in numerous pathological processes in traumatic brain injury (TBI). Growing evidence has indicated that pyroptosis-associated inflammasome is involved in the pathogenesis of TBI. Platelet derived growth factor (PDGF) has been reported to be as a potential therapeutic drug for neurological diseases. However, the roles of PDGF, autophagy and ER stress in pyroptosis have not been elucidated in the TBI. This study investigated the roles of ER stress and autophagy after TBI at different time points. We found that the ER stress and autophagy after TBI were inhibited, and the expressions of pyroptosis-related proteins induced by TBI, including NLRP3, Pro-Caspase1, Caspase1, GSDMD, GSDMD P30, and IL-18, were decreased upon PDGF treatment. Moreover, the rapamycin (RAPA, an autophagy activator) and tunicamycin (TM, an ER stress activator) eliminated the PDGF effect on the pyroptosis after TBI. Interestingly, the sodium 4-phenylbutyrate (4-PBA, an ER stress inhibitor) suppressed autophagy but 3-methyladenine (3-MA, an autophagy inhibitor) not for ER stress. The results revealed that PDGF improved the functional recovery after TBI, and the effects were markedly reversed by TM and RAPA. Taken together, this study provides a new insight that PDGF is a potential therapeutic strategy for enhancing the recovery of TBI.

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Targeting autophagy, oxidative stress, and ER stress for neurodegenerative disease treatment

Cited by 73 publications

References 360 publications

Potential role of TGFΒ and autophagy in early cerebellum development

Potential role of TGFΒ and autophagy in early cerebellum development

Methanolic Extract of Boswellia serrata Gum Protects the Nigral Dopaminergic Neurons from Rotenone-Induced Neurotoxicity

Platelet derived growth factor promotes the recovery of traumatic brain injury by inhibiting endoplasmic reticulum stress and autophagy-mediated pyroptosis

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