Sirt1 improves heart failure through modulating the NF-κB p65/microRNA-155/BNDF signaling cascade

Lin, Bin; Zhao, Hui; Li, Li; Zhang, Zhenzhen; Jiang, Nan; Yang, Xiaowei; Zhang, Tao; Lian, Bowen; Liu, Yaokai; Zhang, Chi; Wang, Jiaxiang; Wang, Feng; Feng, Deguang; Xu, Jing

doi:10.18632/aging.103640

Cited by 35 publications

(21 citation statements)

References 47 publications

(56 reference statements)

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“…The reduced expression of SIRT1 is consistent with the increased levels of acetylation found in heart failure [61]. Overexpression of SIRT1 exhibits protective effects against HF, including increased cell viability, reduced apoptosis, and improved heart function in a rat model [62]. These beneficial effects of SIRT1 are mediated via the activation of eNOS, and the synergism between SIRT1 and eNOS contributes to maintaining endothelial function through positive feedback mechanisms [58].…”

Section: Interaction Between Sirt1 and Enossupporting

confidence: 56%

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Regulation of miRNAs by Natural Antioxidants in Cardiovascular Diseases: Focus on SIRT1 and eNOS

Lee

2021

Antioxidants

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Cardiovascular diseases (CVDs) are the most common cause of morbidity and mortality worldwide. The potential benefits of natural antioxidants derived from supplemental nutrients against CVDs are well known. Remarkably, natural antioxidants exert cardioprotective effects by reducing oxidative stress, increasing vasodilation, and normalizing endothelial dysfunction. Recently, considerable evidence has highlighted an important role played by the synergistic interaction between endothelial nitric oxide synthase (eNOS) and sirtuin 1 (SIRT1) in the maintenance of endothelial function. To provide a new perspective on the role of natural antioxidants against CVDs, we focused on microRNAs (miRNAs), which are important posttranscriptional modulators in human diseases. Several miRNAs are regulated via the consumption of natural antioxidants and are related to the regulation of oxidative stress by targeting eNOS and/or SIRT1. In this review, we have discussed the specific molecular regulation of eNOS/SIRT1-related endothelial dysfunction and its contribution to CVD pathologies; furthermore, we selected nine different miRNAs that target the expression of eNOS and SIRT1 in CVDs. Additionally, we have summarized the alteration of miRNA expression and regulation of activities of miRNA through natural antioxidant consumption.

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Section: Interaction Between Sirt1 and Enossupporting

confidence: 56%

“…The in vivo myocardial injury model showed consistent results, indicating that increased miR-155 expression and negatively regulated SIRT1 expression were involved [ 101 ]. In HF rats, increased expression of miR-155 and attenuated expression of SIRT1 lead to the occurrence of ventricular dysfunction [ 62 ].…”

Section: Cvd-related Mirnas Target Enos and Sirt1mentioning

confidence: 99%

Regulation of miRNAs by Natural Antioxidants in Cardiovascular Diseases: Focus on SIRT1 and eNOS

Lee

2021

Antioxidants

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“…Moreover, Sirt1 deacetylates NF-κB to hampers its transcriptional activity. As an example, Sirt1 overexpression impedes NF-κB acetylation, thereby improving cardiac function and reducing apoptosis in cardiomyocytes [ 21 ]. Tet methylcytosine dioxygenase 1 (TET1) is a demethylase that contributes to reducing DNA methylation levels and the expression of specific genes associated with inflammation [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine prevents cardiomyocytes from hypoxia/reoxygenation injury via modulating tetmethylcytosine dioxygenase 1-mediated DNA demethylation of Sirtuin1

et al. 2022

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Myocardial hypoxia/reoxygenation (H/R) injury is a common pathological change in patients with acute myocardial infarction undergoing reperfusion therapy. Dexmedetomidine (DEX) has been found to substantially improve ischemia-mediated cell damage. Here, we focus on probing the role and mechanism of DEX in ameliorating myocardial H/R injury. Oxygen–glucose deprivation and reoxygenation (OGD/R) were applied to construct the H/R injury model in human myocardial cell lines. After different concentrations of DEX’s treatment, cell counting kit-8 (CCK-8) assay and BrdU assay were employed to test cell viability. The profiles of apoptosis-related proteins Bcl2, Bax, Bad and Caspase3, 8, 9 were determined by Western blot (WB). The expression of inflammatory factors interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) was checked by reverse transcription-polymerase chain reaction (RT-PCR). By conducting WB, we examined the expression of NF-κB, Sirt1, Tet methylcytosine dioxygenase 1 (TET1) and DNA methylation-related proteins (DNA methyltransferase 1, DNMT1; DNA methyltransferase 3 alpha, DNMT3A; and DNA methyltransferase 3 beta, DNMT3B). Our data showed that OGD/R stimulation distinctly hampered the viability and elevated apoptosis and inflammatory factor expression in cardiomyocytes. DEX treatment notably impeded myocardial apoptosis and inflammation and enhanced cardiomyocyte viability. OGD/R enhanced total DNA methylation levels in cardiomyocytes, while DEX curbed DNA methylation. In terms of mechanism, inhibiting TET1 or Sirtuin1 (Sirt1) curbed the DEX-mediated myocardial protection. TET1 strengthened demethylation of the Sirt1 promoter and up-regulated Sirt1. DEX up-regulates Sirt1 by accelerating TET1 and mediating demethylation of the Sirt1 promoter and improves H/R-mediated myocardial injury.

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“…If we consider clinical conditions in which supplemental CoQ10 has been most often employed with some worthwhile efficacy—congestive heart failure, hypertension, and periodontal disease59–64—measures which positively modulate Sirt1 activity have been shown to have a beneficial influence in rodent models of these syndromes, whereas the converse is also true 65–73…”

Section: Enhanced Sirt1 Activity May Explain Some Benefits Of Coq10 S...mentioning

confidence: 99%

Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity

2022

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For reasons that remain unclear, endogenous synthesis and tissue levels of coenzyme Q10 (CoQ10) tend to decline with increasing age in at least some tissues. When CoQ10 levels are sufficiently low, this compromises the efficiency of the mitochondrial electron transport chain, such that production of superoxide by site 2 increases and the rate of adenosine triphosphate production declines. Moreover, CoQ10 deficiency can be expected to decrease activities of Sirt1 and Sirt3 deacetylases, believed to be key determinants of health span. Reduction of the cytoplasmic and mitochondrial NAD+/NADH ratio consequent to CoQ10 deficit can be expected to decrease the activity of these deacetylases by lessening availability of their obligate substrate NAD+. The increased oxidant production induced by CoQ10 deficiency can decrease the stability of Sirt1 protein by complementary mechanisms. And CoQ10 deficiency has also been found to lower mRNA expression of Sirt1. An analysis of the roles of Sirt1/Sirt3 in modulation of cellular function helps to rationalise clinical benefits of CoQ10 supplementation reported in heart failure, hypertension, non-alcoholic fatty liver disease, metabolic syndrome and periodontal disease. Hence, correction of CoQ10 deficiency joins a growing list of measures that have potential for amplifying health protective Sirt1/Sirt3 activities.

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Sirt1 improves heart failure through modulating the NF-κB p65/microRNA-155/BNDF signaling cascade

Cited by 35 publications

References 47 publications

Regulation of miRNAs by Natural Antioxidants in Cardiovascular Diseases: Focus on SIRT1 and eNOS

Regulation of miRNAs by Natural Antioxidants in Cardiovascular Diseases: Focus on SIRT1 and eNOS

Dexmedetomidine prevents cardiomyocytes from hypoxia/reoxygenation injury via modulating tetmethylcytosine dioxygenase 1-mediated DNA demethylation of Sirtuin1

Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity

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