Sirtuins in Brain Aging and Neurological Disorders

Qadir, Muhammad Imran; Anwar, Sidra

doi:10.1615/critreveukaryotgeneexpr.2017019532

Cited by 24 publications

(11 citation statements)

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“…The well-known evolutionary conserved enzymes, that act as deacetylases and ribosyltransferases, are represented by Sirtuins. Based on the different intracellular localizations it is possible distinguish in mammalian 7 sirtuins, which participate to several cell functions such as DNA damage repair, cell cycle, metabolic response to nutrient availability and protection from neurological degeneration [ 189 , 190 , 191 ]. SIRT1 is predominantly nuclear protein but it has been demonstrated that it is able to translocate rapidly from nucleus to cytoplasm, depending on the cellular type and energy status of cell [ 190 ].…”

Section: Genetic Impact On Agingmentioning

confidence: 99%

The Impact of Aging on Cardio and Cerebrovascular Diseases

Izzo

Carrizzo

Alfano

et al. 2018

IJMS

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A growing number of evidences report that aging represents the major risk factor for the development of cardio and cerebrovascular diseases. Understanding Aging from a genetic, biochemical and physiological point of view could be helpful to design a better medical approach and to elaborate the best therapeutic strategy to adopt, without neglecting all the risk factors associated with advanced age. Of course, the better way should always be understanding risk-to-benefit ratio, maintenance of independence and reduction of symptoms. Although improvements in treatment of cardiovascular diseases in the elderly population have increased the survival rate, several studies are needed to understand the best management option to improve therapeutic outcomes. The aim of this review is to give a 360° panorama on what goes on in the fragile ecosystem of elderly, why it happens and what we can do, right now, with the tools at our disposal to slow down aging, until new discoveries on aging, cardio and cerebrovascular diseases are at hand.

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Section: Genetic Impact On Agingmentioning

confidence: 99%

The Impact of Aging on Cardio and Cerebrovascular Diseases

Izzo

Carrizzo

Alfano

et al. 2018

IJMS

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“…SIRT1 has a variety of physiological effects in many diseases, including cancer, metabolic diseases, and degenerative diseases (Haigis & Sinclair, 2010). It is abundant in brain tissue, and its role in the central nervous system has been extensively studied (Qadir & Anwar, 2017).…”

Section: Introductionmentioning

confidence: 99%

Activation of silent information regulator 1 exerts a neuroprotective effect after intracerebral hemorrhage by deacetylating NF‐κB/p65

Deng

Zhou

Huang

et al. 2020

Journal of Neurochemistry

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Nuclear factor (NF)-κB-mediated neuroinflammation is an important mechanism of intracerebral hemorrhage (ICH)-induced neurotoxicity. Silent information regulator 1 (SIRT1) plays a multi-protective effect in a variety of diseases by deacetylating and inhibiting NF-κB/p65. However, the role of SIRT1 in brain damage following ICH remains unclear. We hypothesized that SIRT1 can protect against ICH-induced brain damage by inhibiting neuroinflammation through deacetylating NF-κB/p65. The ICH model was induced in vivo (with collagenase) and in vitro (with hemoglobin).Resveratrol and Ex527 were administered to activate or inhibit SIRT1, respectively.Western blot, immunohistochemistry, and immunofluorescence assays were performed to detect the expression of SIRT1 and p65. Enzyme-linked immunosorbent assays (ELISAs) were used to explore tumor necrosis factor (TNF)-α and interleukin (IL)-1β release. The neurological score, brain water content, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and brain hemoglobin content were determined to evaluate the neuroprotective effect of SIRT1. SIRT1 expression was decreased, whereas the level of acetylated p65 (Ac-p65) was elevated after ICH in vivo. Moreover, hemoglobin treatment decreased the expression of SIRT1 in vitro. Activation of SIRT1 by resveratrol had a neuroprotective effect, along with decreased levels of Ac-p65, IL-1β, TNF-α, and apoptosis after ICH. The effect of resveratrol was abolished by the SIRT1 inhibitor Ex527. Our results are consistent with the hypothesis that SIRT1 exerts a neuroprotective effect after ICH by deacetylating p65 to inhibit the NF-κB-dependent inflammatory response.

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“…Silent mating type information regulation 2 homolog 1 (SIRT1) is an NAD + -dependent deacetylase (Cohen et al, 2004; Bordone and Guarente, 2005). In the brain, SIRT1 is mainly expressed in neurons and has numerous biological functions, including regulation differentiation, metabolism, cell survival, and aging (Qadir and Anwar, 2017). It has been reported that SIRT1 activation attenuates hyperglycemia and plays an important mediatory role in treating diabetic complication (Li X. N. et al, 2017; Zhang Q. et al, 2018; Zhang Y. et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux via Up-regulation of SIRT1

Chen

Wang

et al. 2019

Front. Mol. Neurosci.

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Hyperglycemia, a key characteristic and risk factor for diabetes mellitus (DM), causes neuronal senescence. Hydrogen sulfide (H 2 S) is a novel neuroprotectant. The present work was to investigate the potential effect of H 2 S on hyperglycemia-induced neuronal senescence and the underlying mechanisms. We found that NaHS, a donor of H 2 S, inhibited high glucose (HG)-induced cellular senescence in HT22 cells (an immortalized mouse hippocampal cell line), as evidenced by a decrease in the number of senescence associated-β-galactosidase (SA-β-gal) positive cells, increase in the growth of cells, and down-regulations of senescence mark proteins, p16 INK4a and p21 CIP1 . NaHS improved the autophagic flux, which is judged by a decrease in the amount of intracellular autophagosome as well as up-regulations of LC3II/I and P62 in HG-exposed HT22 cells. Furthermore, blocked autophagic flux by chloroquine (CQ) significantly abolished NaHS-exerted improvement in the autophagic flux and suppression in the cellular senescence of GH-exposed HT22 cells, which indicated that H 2 S antagonizes HG-induced neuronal senescence by promoting autophagic flux. We also found that NaHS up-regulated the expression of silent mating type information regulation 2 homolog 1 (SIRT1), an important anti-aging protein, in HG-exposed HT22 cells. Furthermore, inhibition of SIRT1 by sirtinol reversed the protection of H 2 S against HG-induced autophagic flux blockade and cellular senescence in HT22 cells. These data indicated that H 2 S protects HT22 cells against HG-induced neuronal senescence by improving autophagic flux via up-regulation of SIRT1, suggesting H 2 S as a potential treatment strategy for hyperglycemia-induced neuronal senescence and neurotoxicity.

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Sirtuins in Brain Aging and Neurological Disorders

Cited by 24 publications

References 0 publications

The Impact of Aging on Cardio and Cerebrovascular Diseases

The Impact of Aging on Cardio and Cerebrovascular Diseases

Activation of silent information regulator 1 exerts a neuroprotective effect after intracerebral hemorrhage by deacetylating NF‐κB/p65

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux via Up-regulation of SIRT1

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