Sirtuin 3 promotes microglia migration by upregulating CX3CR1

Cao, Runjing; Li, Shiping; Yin, Jun; Guo, Li; Shi, Jiong

doi:10.1080/19336918.2019.1629224

Cited by 16 publications

(15 citation statements)

References 24 publications

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“…Overexpression of SIRT3 after ischemia leads to the upregulation of CX3CR1 expression, which promotes G protein-dependent migration of microglia ( 75 ). Thus, activation of the CX3CL1/CX3CR1 signaling axis in the early stage after ischemic stroke promotes microglial activation, migration, intrinsic phagocytosis, the release of pro-inflammatory substances, and exacerbate nerve injury.…”

Section: Mechanisms Of Microglial Activation and Polarization After Strokementioning

confidence: 99%

Effects of Microglial Activation and Polarization on Brain Injury After Stroke

et al. 2021

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Stroke is one of the most common causes of death worldwide. The subsequent development of neuroinflammation and brain edema dramatically increases the risks associated with stroke, leading to a substantial increase in mortality. Although considerable progress has been made in improving cerebral perfusion in the acute phase of stroke, effective treatment options for the subacute and chronic phases associated with cerebral infarction are limited. Microglia, the innate immune cells of the central nervous system (CNS), can be activated and polarized to take on different phenotypes in response to stimulations associated with stroke, including pro-inflammatory and anti-inflammatory phenotypes, which affect the prognosis of stroke. Therefore, investigation of the activation and polarizing mechanisms of microglia plays a critical role in treating stroke. The aim of this article was to investigate the significance of microglial phenotype regulation in stroke treatment by summarizing the activation, polarizing mechanisms, and general microglia characteristics.

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Section: Mechanisms Of Microglial Activation and Polarization After Strokementioning

confidence: 99%

Effects of Microglial Activation and Polarization on Brain Injury After Stroke

et al. 2021

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“…In aged mice with postoperative cognitive dysfunction, microglial activation and elevated proinflammatory cytokine levels were found to be associated with decreased SOD and Sirt3 expression in the hippocampus ( Liu et al, 2021 ). In addition, Sirt3 promoted microglial migration to the site of the lesion by upregulating the fractalkine receptor CX3CR1 in mice with ischemic stroke ( Cao et al, 2019 ).…”

Section: Role Of Sirtuins In Neuroinflammationmentioning

confidence: 99%

Sirtuins as Potential Therapeutic Targets for Mitigating Neuroinflammation Associated With Alzheimer’s Disease

Fernando

Wijayasinghe

2021

Front. Cell. Neurosci.

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Alzheimer’s disease (AD) is the most common neurodegenerative disorder, which is associated with memory deficit and global cognitive decline. Age is the greatest risk factor for AD and, in recent years, it is becoming increasingly appreciated that aging-related neuroinflammation plays a key role in the pathogenesis of AD. The presence of β-amyloid plaques and neurofibrillary tangles are the primary pathological hallmarks of AD; defects which can then activate a cascade of molecular inflammatory pathways in glial cells. Microglia, the resident macrophages in the central nervous system (CNS), are the major triggers of inflammation; a response which is typically intended to prevent further damage to the CNS. However, persistent microglial activation (i.e., neuroinflammation) is toxic to both neurons and glia, which then leads to neurodegeneration. Growing evidence supports a central role for sirtuins in the regulation of neuroinflammation. Sirtuins are NAD+-dependent protein deacetylases that modulate a number of cellular processes associated with inflammation. This review examines the latest findings regarding AD-associated neuroinflammation, mainly focusing on the connections among the microglial molecular pathways of inflammation. Furthermore, we highlight the biology of sirtuins, and their role in neuroinflammation. Suppression of microglial activity through modulation of the sirtuin activity has now become a key area of research, where progress in therapeutic interventions may slow the progression of Alzheimer’s disease.

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“…LPSinduced inflammatory activation of BV-2 microglial cells was inhibited by treatment with ketone bodies, which was attributed to inhibition of HDAC (Huang et al, 2018). Another evidence of epigenetic regulation of microglial metabolism comes from the study evaluating the anti-inflammatory activity of sirtuin 3 (SIRT3) (Cao et al, 2019). Silent mating-type information regulator 2 homolog (SIRTs) are known to regulate the genes responsible for metabolic enzymes (Finley and Haigis, 2012).…”

Section: Modulation Of Glial Metabolism As a Therapeutic Strategymentioning

confidence: 99%

“…Silent mating-type information regulator 2 homolog (SIRTs) are known to regulate the genes responsible for metabolic enzymes (Finley and Haigis, 2012). SIRT3 reduced the production of superoxide dismutase and increased the migratory potential of microglia cells in vitro (Cao et al, 2019). Upregulation of SIRT3 in astrocytes also inhibited their inflammatory activation, highlighting the possibility of metabolic regulation by targeting epigenetics (Yang et al, 2017).…”

Section: Modulation Of Glial Metabolism As a Therapeutic Strategymentioning

confidence: 99%

Metabolic Regulation of Glial Phenotypes: Implications in Neuron–Glia Interactions and Neurological Disorders

Afridi

Kim

Rahman

et al. 2020

Front. Cell. Neurosci.

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Glial cells are multifunctional, non-neuronal components of the central nervous system with diverse phenotypes that have gained much attention for their close involvement in neuroinflammation and neurodegenerative diseases. Glial phenotypes are primarily characterized by their structural and functional changes in response to various stimuli, which can be either neuroprotective or neurotoxic. The reliance of neurons on glial cells is essential to fulfill the energy demands of the brain for its proper functioning. Moreover, the glial cells perform distinct functions to regulate their own metabolic activities, as well as work in close conjunction with neurons through various secreted signaling or guidance molecules, thereby constituting a complex network of neuron-glial interactions in health and disease. The emerging evidence suggests that, in disease conditions, the metabolic alterations in the glial cells can induce structural and functional changes together with neuronal dysfunction indicating the importance of neuron-glia interactions in the pathophysiology of neurological disorders. This review covers the recent developments that implicate the regulation of glial phenotypic changes and its consequences on neuron-glia interactions in neurological disorders. Finally, we discuss the possibilities and challenges of targeting glial metabolism as a strategy to treat neurological disorders.

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Sirtuin 3 promotes microglia migration by upregulating CX3CR1

Cited by 16 publications

References 24 publications

Effects of Microglial Activation and Polarization on Brain Injury After Stroke

Effects of Microglial Activation and Polarization on Brain Injury After Stroke

Sirtuins as Potential Therapeutic Targets for Mitigating Neuroinflammation Associated With Alzheimer’s Disease

Metabolic Regulation of Glial Phenotypes: Implications in Neuron–Glia Interactions and Neurological Disorders

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