Knockdown of GSK3β increases basal autophagy and AMPK signalling in nutrient-laden human aortic endothelial cells

Weikel, Karen A.; Cacicedo, José M.; Ruderman, Neil B.; Ido, Yasuo

doi:10.1042/bsr20160174

Cited by 46 publications

(35 citation statements)

References 98 publications

(133 reference statements)

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“…Further complicating the matter, the interaction of AMPK with PP2A and GSK3β is not only one-way street; these downstream molecules also negatively regulate the activity of AMPK. It is evident that GSK3β inhibits the activity of AMPK [153]. is backward effect produces antitauopathy effect because AMPK inhibits GSK3β and GSK3β inhibition activates AMPK.…”

Section: Ampk and Tauopathymentioning

confidence: 99%

The Bewildering Effect of AMPK Activators in Alzheimer’s Disease: Review of the Current Evidence

Assefa

Tafere

Wondafrash

et al. 2020

BioMed Research International

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Alzheimer’s disease is a multifactorial neurodegenerative disease characterized by progressive cognitive dysfunction. It is the most common form of dementia. The pathologic hallmarks of the disease include extracellular amyloid plaque, intracellular neurofibrillary tangles, and oxidative stress, to mention some of them. Despite remarkable progress in the understanding of the pathogenesis of the disease, drugs for cure or disease-modifying therapy remain somewhere in the distance. From recent time, the signaling molecule AMPK is gaining enormous attention in the AD drug research. AMPK is a master regulator of cellular energy metabolism, and recent pieces of evidence show that perturbation of its function is highly ascribed in the pathology of AD. Several drugs are known to activate AMPK, but their effect in AD remains to be controversial. In this review, the current shreds of evidence on the effect of AMPK activators in Aβ accumulation, tau aggregation, and oxidative stress are addressed. Positive and negative effects are reported with regard to Aβ and tauopathy but only positive in oxidative stress. We also tried to dissect the molecular interplays where the bewildering effects arise from.

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Section: Ampk and Tauopathymentioning

confidence: 99%

The Bewildering Effect of AMPK Activators in Alzheimer’s Disease: Review of the Current Evidence

Assefa

Tafere

Wondafrash

et al. 2020

BioMed Research International

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“…In regards to autophagy, FoxO proteins may be protective. Some studies suggest that FoxO activity, such as FoxO1, can function to increase basal autophagy and reduce atherogenesis (53, 54). Ectopic expression of FoxO1 enhances autophagy and toxic mHtt protein clearance in neuronal cell cultures (55).…”

Section: Foxo Transcription Factors and Cell Deathmentioning

confidence: 99%

Forkhead Transcription Factors: Formulating a FOXO Target for Cognitive Loss

Maiese¹

2018

CNR

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“…Increased FoxO activity, such as with FoxO1, can function to increase basal autophagy and reduce atherogenesis (56, 223). Ectopic expression of FoxO1 enhances autophagy and increases toxic Huntington’s disease Huntingtin (mHtt) protein clearance in neuronal cell cultures (224).…”

Section: Foxo Transcription Factorsmentioning

confidence: 99%

Novel Treatment Strategies for the Nervous System: Circadian Clock Genes, Non-coding RNAs, and Forkhead Transcription Factors

Maiese¹

2018

CNR

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BACKGROUND With the global increase in life span expectancy, neurodegenerative disorders continue to affect an ever increasing number of individuals throughout the world. New treatment strategies for neurodegenerative diseases are desperately required given the lack of current treatment modalities. METHODS Here we examine novel strategies for neurodegenerative disorders that include circadian clock genes, non-coding ribonucleic acids (RNAs), and the mammalian forkhead transcription factors of the O class (FoxOs). RESULTS Circadian clock genes, non-coding RNAs, and FoxOs offer exciting prospects to potentially limit or remove the significant disability and death associated with neurodegenerative disorders. Each of these pathways have an intimate relationship with the programmed death pathways of autophagy and apoptosis and share a common link to the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) and the mechanistic target of rapamycin (mTOR). Circadian clock genes are necessary to modulate autophagy, limit cognitive loss, and prevent neuronal injury. Non-coding RNAs can control neuronal stem cell development and neuronal differentiation and offer protection against vascular disease such as atherosclerosis. FoxOs provide exciting prospects to block neuronal apoptotic death and to activate pathways of autophagy to remove toxic accumulations in neurons that can lead to neurodegenerative disorders. CONCLUSIONS Continued work with circadian clock genes, non-coding RNAs, and FoxOs can offer new prospects and hope for the development of vital strategies for the treatment of neurodegenerative diseases. These innovative investigative avenues have the potential to significantly limit disability and death from these devastating disorders.

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Knockdown of GSK3β increases basal autophagy and AMPK signalling in nutrient-laden human aortic endothelial cells

Abstract: Suppression of the enzyme glycogen synthase kinase 3β (GSK3β) increases both the turnover of damaged cellular material and the activity of the enzyme AMP-activated protein kinase (AMPK) to potentially attenuate the damage inflicted by excess sugar and fat on blood vessels.

Cited by 46 publications

References 98 publications

The Bewildering Effect of AMPK Activators in Alzheimer’s Disease: Review of the Current Evidence

The Bewildering Effect of AMPK Activators in Alzheimer’s Disease: Review of the Current Evidence

Forkhead Transcription Factors: Formulating a FOXO Target for Cognitive Loss

Novel Treatment Strategies for the Nervous System: Circadian Clock Genes, Non-coding RNAs, and Forkhead Transcription Factors

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