Duck Oil-loaded Nanoemulsion Inhibits Senescence of Angiotensin
                    II-treated Vascular Smooth Muscle Cells by Upregulating SIRT1

Kang, Eun Sil; Kim, Hyo Juong; Han, Sung Gu; Seo, Han Geuk

doi:10.5851/kosfa.2019.e93

Cited by 12 publications

(6 citation statements)

References 41 publications

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“…Later on, as DNs damage progress, the antioxidant capacity is reduced with the augmentation of oxidative stress injury (Qi et al 2018 ). It has been shown that SIRT1 prevents the development of endothelial dysfunction through attenuation progression of oxidative stress by multiple mechanisms including SIRT1/SOD, SIRT1/FOXO, SIRT1/eNOs, and SIRT1/NF-κB (Kang et al 2020 ). In addition, increasing ROS and oxidative stress by the aging process attenuate expression and functional activity of SIRT1 with further progress of oxidative stress and activation of inflammatory signaling pathway NF-κB leading to advanced inflammatory and oxidative stress injury (Bouchez and Devin 2019 ).…”

Section: Mechanistic Role Of Sirt1 In Pdmentioning

confidence: 99%

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

et al. 2022

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Silent information regulator (SIRT) has distinctive enzymatic activities and physiological functions to control cell-cycle progression, gene expression, and DNA stability by targeting histone and non-histone proteins. SIRT1 enhances synaptic formation and synaptic activity, and therefore, can reduce the progression of various degenerative brain diseases including Parkinson’s disease (PD). SIRT1 activity is decreased by aging with a subsequent increased risk for the development of degenerative brain diseases. Inhibition of SIRT1 promotes inflammatory reactions since SIRT1 inhibits transcription of nuclear factor kappa B (NF-κB) which also inhibits SIRT1 activation via activation of microRNA and miR-34a which reduce NAD synthesis. SIRT1 is highly expressed in microglia as well as neurons, and has antioxidant and anti-inflammatory effects. Therefore, this review aimed to find the possible role of SIRT1 in PD neuropathology. SIRT1 has neuroprotective effects; therefore, downregulation of SIRT1 during aging promotes p53 expression and may increase the vulnerability of neuronal cell deaths. PD neuropathology is linked with the sequence of inflammatory changes and the release of pro-inflammatory cytokines due to the activation of inflammatory signaling pathways. In addition, oxidative stress, inflammatory disorders, mitochondrial dysfunction, and apoptosis contribute mutually to PD neuropathology. Thus, SIRT1 and SIRT1 activators play a crucial role in the mitigation of PD neuropathology through the amelioration of oxidative stress, inflammatory disorders, mitochondrial dysfunction, apoptosis, and inflammatory signaling pathways.

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Section: Mechanistic Role Of Sirt1 In Pdmentioning

confidence: 99%

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

et al. 2022

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“…9 Numerous studies have demonstrated the potential of SIRT1 upregulation using both natural and synthetic compounds as a strategy for inhibiting cellular senescence and prolonging cellular longevity. 10,11 Dipeptidyl peptidase-4 (DPP)-4 is an exopeptidase enzyme expressed on the surface VSMCs that regulates glucagon-like peptide (GLP)-1 activity and has been shown to be involved in vascular flexibility. 12 GLP-1 is an incretin hormone secreted by intestinal L cells that activates the GLP-1 receptor (GLP-1R) to promote postprandial insulin secretion, among other functions.…”

Section: Introductionmentioning

confidence: 99%

“…Silent information-regulator 1 (SIRT1) is a NAD-dependent deacetylase that plays an important role in regulating the cell cycle by suppressing the acetylation of p53 protein . Numerous studies have demonstrated the potential of SIRT1 upregulation using both natural and synthetic compounds as a strategy for inhibiting cellular senescence and prolonging cellular longevity. , …”

Section: Introductionmentioning

confidence: 99%

Omarigliptin Prevents TNF-α-Induced Cellular Senescence in Rat Aorta Vascular Smooth Muscle Cells

Zhang

Yuan

Zhou

et al. 2021

Chem. Res. Toxicol.

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Cellular senescence is one of the most significant factors involved in aging and age-related diseases. Senescence of vascular smooth muscle cells (VSMCs) adversely affects the function of the cardiovascular system and contributes to the development of atherosclerosis, hypertension, and other cardiovascular diseases. Glucagon-like peptide-1 (GLP-1) is an important incretin hormone involved in insulin release and vascular tone. GLP-1 is quickly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4). Omarigliptin is a new DPP-4 inhibitor that has demonstrated anti-inflammatory and antioxidative stress properties. In the present study, we investigated the effects of the selective DPP-4 inhibitor omarigliptin (OMG) on VSMCs exposed to insult from tumor necrosis factor-α (TNF-α), one of the main inflammatory signaling molecules involved in cellular senescence. We found that OMG could suppress TNF-α-induced expression of pro-inflammatory cytokines (interleukin-1β (IL-1β), IL-6, and IL-8) and inhibit oxidative stress by reducing the production of H 2 O 2 and protein carbonyl. OMG ameliorated the increase in senescence-associated β-galactosidase (SA-β-gal) and telomerase activity induced by TNF-α. The plasminogen activator inhibitor-1 (PAI-1)/p53/p21 pathway is a key inducer of cellular senescence. OMG ameliorated the acetylation of p53 at lysine 382 (K382) and subsequent activation of p21 via inhibition of PAI-1. Importantly, our experiments revealed that blockage of silent information-regulator 1 (SIRT1) abolished the inhibitory effects of OMG on p53 acetylation, SA-β-gal activity, and telomerase activity in VSMCs. These results suggest that OMG may have the potential to delay or prevent the progression of age-related cardiovascular diseases by modulating the activity of SIRT1.

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“…Sirtuin 1 (SIRT1) is a member of the Sirtuin family of class III histone deacetylase enzymes, which plays a critical role in modulating cell senescence [ 6 ], cell proliferation [ 7 ], and inflammation responses [ 8 ]. Extensive studies have shown that SIRT1 overexpression protects human vessels against stress senescence of VSMCs stimulated by inflammation [ 9 , 10 ], thus improving the normal function of VSMCs, inhibiting vascular inflammation and plaque formation [ 3 ]. At the mechanistic level, p53 is a known senescence-promoting protein and is a downstream transcription factor regulated by SIRT1 [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Paeonol Attenuates Atherosclerosis by Inhibiting Vascular Smooth Muscle Cells Senescence via SIRT1/P53/TRF2 Signaling Pathway

Zhou,

Ma,

Gao

et al. 2024

Molecules

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Atherosclerosis is a chronic inflammatory disease leading to various vascular diseases. Vascular smooth muscle cell (VSMC) senescence promotes atherosclerotic inflammation and the formation of plaque necrosis core, in part through telomere damage mediated by a high-fat diet. Our previous research found that paeonol, a potential anti-inflammatory agent extracted from Cortex Moutan, could significantly improve VSMCs dysfunction. However, the impact of paeonol on the senescence of VSMCs remains unexplored. This study presents the protective effects of paeonol on VSMCs senescence, and its potential activity in inhibiting the progression of atherosclerosis in vivo and in vitro. Sirtuin 1 (SIRT1) is a nuclear deacetylase involved in cell proliferation, senescence, telomere damage, and inflammation. Here, SIRT1 was identified as a potential target of paeonol having anti-senescence and anti-atherosclerosis activity. Mechanistic studies revealed that paeonol binds directly to SIRT1 and then activates the SIRT1/P53/TRF2 pathway to inhibit VSMCs senescence. Our results suggested that SIRT1-mediated VSMCs senescence is a promising druggable target for atherosclerosis, and that pharmacological modulation of the SIRT1/P53/TRF2 signaling pathway by paeonol is of potential benefit for patients with atherosclerosis.

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Duck Oil-loaded Nanoemulsion Inhibits Senescence of Angiotensin II-treated Vascular Smooth Muscle Cells by Upregulating SIRT1

Cited by 12 publications

References 41 publications

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

Omarigliptin Prevents TNF-α-Induced Cellular Senescence in Rat Aorta Vascular Smooth Muscle Cells

Paeonol Attenuates Atherosclerosis by Inhibiting Vascular Smooth Muscle Cells Senescence via SIRT1/P53/TRF2 Signaling Pathway

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