SIRT3 Mediates the Antioxidant Effect of Hydrogen Sulfide in Endothelial Cells

Xie, Liping; Feng, Hailan; Li, Sha; Meng, Guoliang; Liu, Shangmin; Tang, Xin; Ma, Yan; Han, Yi; Xiao, Yuchen; Gu, Yue; Shao, Yongfeng; Park, Chung Min; Xian, Ming; Huang, Yü; Ferro, Albert; Wang, Rui; Moore, Philip K.; Wang, Hong; Ji, Yong

doi:10.1089/ars.2015.6331

Cited by 102 publications

(59 citation statements)

References 54 publications

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“…Treatment with NaHS enhanced the SIRT1 deacetylase activity in human umbilical vein endothelial cells [119, 121]. In addition, increases in the expression of SIRT1 [119, 120], SIRT3 [180, 192] and SIRT6 [180, 193] were shown after treatment with H 2 S.…”

Section: Hydrogen Sulfide and Agingmentioning

confidence: 99%

The role of hydrogen sulfide in aging and age-related pathologies

Perridon

Leuvenink

Hillebrands

et al. 2016

Aging

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When humans grow older, they experience inevitable and progressive loss of physiological function, ultimately leading to death. Research on aging largely focuses on the identification of mechanisms involved in the aging process. Several proposed aging theories were recently combined as the ‘hallmarks of aging’. These hallmarks describe (patho-)physiological processes that together, when disrupted, determine the aging phenotype. Sustaining evidence shows a potential role for hydrogen sulfide (H2S) in the regulation of aging.Nowadays, H2S is acknowledged as an endogenously produced signaling molecule with various (patho-) physiological effects. H2S is involved in several diseases including pathologies related to aging. In this review, the known, assumed and hypothetical effects of hydrogen sulfide on the aging process will be discussed by reviewing its actions on the hallmarks of aging and on several age-related pathologies.

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Section: Hydrogen Sulfide and Agingmentioning

confidence: 99%

The role of hydrogen sulfide in aging and age-related pathologies

Perridon

Leuvenink

Hillebrands

et al. 2016

Aging

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show abstract

“…Zhao et al examined the vasoactive effects of H 2 S in rat aortic tissues [63][64][65][66][67][68][69][70]. The report shows a dose-dependent inhibition of H 2 S-induced vasodilation of rat aortic rings by the K ATP channel inhibitor, glibenclamide.…”

Section: Vasodilationmentioning

confidence: 99%

“…Thus, the synthesis of this gasotransmitter is not completely defined and remains an area of active investigation as discussed below. After synthesis and release, H 2 S has effects in the vascular wall that include inhibition of inflammation [13][14][15][16][17], stimulation of angiogenesis [18][19][20][21][22], increased production of endothelium-derived relaxing factors [23][24][25], activation of antioxidant pathways [26], and direct stimulation of vascular smooth muscle cell vasodilation [8,27,28]. These pathways will be discussed below along with a discussion of H 2 S production and activity in several cardiovascular diseases.…”

Section: Introductionmentioning

confidence: 99%

Diabetic keto acidosis as a deceiving presentation to simultaneous aortic and tricuspid infective endocarditis

VP¹,

Ciancerelli²,

Silber³

et al. 2018

Cardiovasc Disord Med

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In the vascular wall, hydrogen sulfide (H 2 S) inhibits inflammation, stimulates angiogenesis, and activates vasodilation. There are multiple sources of H 2 S in the vascular wall, but cystathionine gamma-lyase (CSE) within endothelial cells appears to produce most of the local, vascular H 2 S. Generated H 2 S acts on smooth muscle, endothelial, inflammatory, and adipose cells within the vascular wall and contributes to circulating levels of H 2 S and H 2 S metabolites. H 2 S signaling is generally beneficial with evidence that it inhibits inflammation and protects cells from oxidative stress. H 2 S also stimulates vasodilation and suppresses cytokine generation. Oxidized low-density lipoproteins (oxLDL) and hyperglycemia downregulate the pathway in cultured cells and disease states. Lower plasma and urine levels have been reported in human studies of diabetes, hypertension, and atherosclerosis so that suppression of this system may contribute to vascular disease. Activation of the system or supplementation with exogenous donors of H 2 S appears to protect from vascular and inflammatory diseases. Areas of active research include delineating signal transduction pathways both upstream of CSE and downstream of released H 2 S as well as defining more accurate and user-friendly ways to measure endogenous production.

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“…Besides HUVECs, previous studies from our group demonstrated that H 2 S increased SIRT1 expression to abolish the oxidative stress induced apoptosis in H9c2 cardiomyocytes [70] and previous studies from our group demonstrated [6] found that H 2 S attenuated inflammatory hepcidin partially by promoting SIRT1-mediated STAT3 deacetylation. SIRT3, one of the isoforms of SIRT family, has also been reported that it could be regulated by H 2 S to protect endothelial cells in an antioxidant manner [71]. …”

Section: H2s Epigenetic Regulation Atherosclerosis Is An Important Famentioning

confidence: 99%

Atherosclerosis and the Hydrogen Sulfide Signaling Pathway – Therapeutic Approaches to Disease Prevention

Zj¹,

Wu²,

Guo³

et al. 2017

Cell Physiol Biochem

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Hydrogen sulfide (H₂S) is now admitted as a third gasotransmitter together with nitric oxide (NO) and carbon monoxide (CO), albeit it was originally considered as a foul and poisonous gas. Endogenous H₂S production in mammalian cells is counting on the three enzymes acting on cysteine. Involvement of H₂S in various physiological and pathological processes has been extensively studied in the last fifteen years. Mounting evidence suggests that H₂S is able to protect against atherosclerosis development and progression. Exogenous H₂S supplement has salutary effects on atherogenesis, and reduction of the endogenous H₂S level accelerates atherosclerosis. The anti-atherosclerotic mechanisms of H₂S have been descried in different aspects, including endothelium preservation, antioxidative action, anti-inflammatory responses, vasorelaxation, regulation of ion channels, etc. However, further investigation is still needed to help us gain more insights into the fundamental underlying mechanisms, and that will allow us to design better therapeutic applications of H₂S in the treatment of atherosclerosis.

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SIRT3 Mediates the Antioxidant Effect of Hydrogen Sulfide in Endothelial Cells

Abstract: H2S enhances AP-1 binding activity with the SIRT3 promoter, thereby upregulating SIRT3 expression and ultimately reducing oxidant-provoked vascular endothelial dysfunction. Antioxid. Redox Signal. 24, 329-343.

Cited by 102 publications

References 54 publications

The role of hydrogen sulfide in aging and age-related pathologies

The role of hydrogen sulfide in aging and age-related pathologies

Diabetic keto acidosis as a deceiving presentation to simultaneous aortic and tricuspid infective endocarditis

Atherosclerosis and the Hydrogen Sulfide Signaling Pathway – Therapeutic Approaches to Disease Prevention

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