AMPK Signaling Regulates the Age-Related Decline of Hippocampal Neurogenesis

Wang, Brian Z; Yang, Jane J; Zhang, Hongxia; Smith, Charity; Jin, Kunlin

doi:10.14336/ad.2019.0102

Cited by 33 publications

(26 citation statements)

References 69 publications

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“…AMPK (a serine/threonine protein kinase) is an essential energy sensor engaged in modulating our whole-body level of metabolic energy balance [ 5 , 6 ]. In mammals, AMPK comprises of two isoforms of the α and β subunits each and three isoforms of the γ subunits to form a combination of 12 different αβγ isoforms.…”

Section: Ampk Signalingmentioning

confidence: 99%

“…β-adrenergics could accelerate myocardial fibrosis by downregulating AMPK activity and upregulating β-arrestin 1 in aged mice [ 18 ]. AMPK signaling also participates in the age-related decline of hippocampal neurogenesis [ 6 ], which has been shown to contribute to cognitive impairment. Taken together, these findings suggest that age-related alterations are associated with the AMPK pathway.…”

Section: Ampk Signalingmentioning

confidence: 99%

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Key Signaling Pathways in Aging and Potential Interventions for Healthy Aging

Zhang

Wang

et al. 2021

Cells

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Aging is a fundamental biological process accompanied by a general decline in tissue function. Indeed, as the lifespan increases, age-related dysfunction, such as cognitive impairment or dementia, will become a growing public health issue. Aging is also a great risk factor for many age-related diseases. Nowadays, people want not only to live longer but also healthier. Therefore, there is a critical need in understanding the underlying cellular and molecular mechanisms regulating aging that will allow us to modify the aging process for healthy aging and alleviate age-related disease. Here, we reviewed the recent breakthroughs in the mechanistic understanding of biological aging, focusing on the adenosine monophosphate-activated kinase (AMPK), Sirtuin 1 (SIRT1) and mammalian target of rapamycin (mTOR) pathways, which are currently considered critical for aging. We also discussed how these proteins and pathways may potentially interact with each other to regulate aging. We further described how the knowledge of these pathways may lead to new interventions for antiaging and against age-related disease.

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Section: Ampk Signalingmentioning

confidence: 99%

Section: Ampk Signalingmentioning

confidence: 99%

Key Signaling Pathways in Aging and Potential Interventions for Healthy Aging

Zhang

Wang

et al. 2021

Cells

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“…AMPK is an energy and nutrient sensor activated in response to energy starvation to provide the restoration of ATP level in cells due to switch from anabolic to catabolic metabolism (reviewed by [220][221][222][223]. High AMPK activity is associated with variety of metabolic processes including stimulation of glucose uptake by cells and mitochondrial oxidative metabolism, that is, glucose oxidation, FAO, and OXPHOS.…”

Section: Role Of Ampk In Promoting Cancer Cell Oxidative Metabolismmentioning

confidence: 99%

Metabolic Heterogeneity of Cancer Cells: An Interplay between HIF-1, GLUTs, and AMPK

Moldogazieva

Mokhosoev

Terentiev

2020

Cancers

110

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It has been long recognized that cancer cells reprogram their metabolism under hypoxia conditions due to a shift from oxidative phosphorylation (OXPHOS) to glycolysis in order to meet elevated requirements in energy and nutrients for proliferation, migration, and survival. However, data accumulated over recent years has increasingly provided evidence that cancer cells can revert from glycolysis to OXPHOS and maintain both reprogrammed and oxidative metabolism, even in the same tumor. This phenomenon, denoted as cancer cell metabolic plasticity or hybrid metabolism, depends on a tumor micro-environment that is highly heterogeneous and influenced by an intensity of vasculature and blood flow, oxygen concentration, and nutrient and energy supply, and requires regulatory interplay between multiple oncogenes, transcription factors, growth factors, and reactive oxygen species (ROS), among others. Hypoxia-inducible factor-1 (HIF-1) and AMP-activated protein kinase (AMPK) represent key modulators of a switch between reprogrammed and oxidative metabolism. The present review focuses on cross-talks between HIF-1, glucose transporters (GLUTs), and AMPK with other regulatory proteins including oncogenes such as c-Myc, p53, and KRAS; growth factor-initiated protein kinase B (PKB)/Akt, phosphatidyl-3-kinase (PI3K), and mTOR signaling pathways; and tumor suppressors such as liver kinase B1 (LKB1) and TSC1 in controlling cancer cell metabolism. The multiple switches between metabolic pathways can underlie chemo-resistance to conventional anti-cancer therapy and should be taken into account in choosing molecular targets to discover novel anti-cancer drugs.

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“…Therefore, AMPK may represent a link between memory process and metabolic control [ 89 ]. In addition, increase in AMPK activation with age is a key factor leading to age-related decline of hippocampal neurogenesis and, thus, increased susceptibility to age-associated neurological diseases [ 90 ]. Thus, it is possible to hypothesize that HFD-induced increased activation of AMPK in the hippocampus exacerbates age-related decline, contributing to the synaptic dysfunctions observed in neurodegenerative diseases.…”

Section: Overnutrition and Synaptic Plasticitymentioning

confidence: 99%

Interplay between Peripheral and Central Inflammation in Obesity-Promoted Disorders: The Impact on Synaptic Mitochondrial Functions

Crispino

Trinchese

Penna

et al. 2020

IJMS

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The metabolic dysfunctions induced by high fat diet (HFD) consumption are not limited to organs involved in energy metabolism but cause also a chronic low-grade systemic inflammation that affects the whole body including the central nervous system. The brain has been considered for a long time to be protected from systemic inflammation by the blood–brain barrier, but more recent data indicated an association between obesity and neurodegeneration. Moreover, obesity-related consequences, such as insulin and leptin resistance, mitochondrial dysfunction and reactive oxygen species (ROS) production, may anticipate and accelerate the physiological aging processes characterized by systemic inflammation and higher susceptibility to neurological disorders. Here, we discussed the link between obesity-related metabolic dysfunctions and neuroinflammation, with particular attention to molecules regulating the interplay between energetic impairment and altered synaptic plasticity, for instance AMP-activated protein kinase (AMPK) and Brain-derived neurotrophic factor (BDNF). The effects of HFD-induced neuroinflammation on neuronal plasticity may be mediated by altered brain mitochondrial functions. Since mitochondria play a key role in synaptic areas, providing energy to support synaptic plasticity and controlling ROS production, the negative effects of HFD may be more pronounced in synapses. In conclusion, it will be emphasized how HFD-induced metabolic alterations, systemic inflammation, oxidative stress, neuroinflammation and impaired brain plasticity are tightly interconnected processes, implicated in the pathogenesis of neurological diseases.

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AMPK Signaling Regulates the Age-Related Decline of Hippocampal Neurogenesis

Cited by 33 publications

References 69 publications

Key Signaling Pathways in Aging and Potential Interventions for Healthy Aging

Key Signaling Pathways in Aging and Potential Interventions for Healthy Aging

Metabolic Heterogeneity of Cancer Cells: An Interplay between HIF-1, GLUTs, and AMPK

Interplay between Peripheral and Central Inflammation in Obesity-Promoted Disorders: The Impact on Synaptic Mitochondrial Functions

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