Sirtuins: To Be or Not To Be in Diabetic Cardiomyopathy

Palomer, Xavier; Aguilar-Recarte, David; García, Raquel; Nistal, J. Francisco; Vázquez‐Carrera, Manuel

doi:10.1016/j.molmed.2021.03.004

Cited by 28 publications

(20 citation statements)

References 119 publications

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“…However, the subcellular location and enzymatic functions are varied among these sirtuins (Grootaert and Bennett, 2022). SIRT1, SIRT6, and SIRT7 are sirtuins that reside in the nucleus; SIRT2 is predominantly presented in the cytosol; whereas SIRT3, SIRT4, and SIRT5 are localized in mitochondria (Palomer et al, 2021). The predominant enzymatic activity of sirtuins is deacetylation, which is dependent on NAD + (Wang and Lin, 2021).…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress and inflammation regulation of sirtuins: New insights into common oral diseases

et al. 2022

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Sirtuins are a family of nicotinamide adenine dinucleotide (NAD)+-dependent histone deacetylases, comprising seven members SIRT1-SIRT7. Sirtuins have been extensively studied in regulating ageing and age-related diseases. Sirtuins are also pivotal modulators in oxidative stress and inflammation, as they can regulate the expression and activation of downstream transcriptional factors (such as Forkhead box protein O3 (FOXO3a), nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor-kappa B (NF-κB)) as well as antioxidant enzymes, through epigenetic modification and post-translational modification. Most importantly, studies have shown that aberrant sirtuins are involved in the pathogenesis of infectious and inflammatory oral diseases, and oral cancer. In this review, we provide a comprehensive overview of the regulatory patterns of sirtuins at multiple levels, and the essential roles of sirtuins in regulating inflammation, oxidative stress, and bone metabolism. We summarize the involvement of sirtuins in several oral diseases such as periodontitis, apical periodontitis, pulpitis, oral candidiasis, oral herpesvirus infections, dental fluorosis, and oral cancer. At last, we discuss the potential utilization of sirtuins as therapeutic targets in oral diseases.

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Section: Introductionmentioning

confidence: 99%

Oxidative stress and inflammation regulation of sirtuins: New insights into common oral diseases

et al. 2022

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“…Furthermore, the molecular mechanism of the RvE1 and LXA4 combination on NF‐κB suppression was also investigated in this study. SIRTs are a highly conserved family of deacetylases, of which the enzymatic activities are strictly regulated by NAD+ 52,53 . In LPS‐induced DPFs in vitro, we found that the expression of SIRT1 and SIRT6, which are located in the nucleus, was significantly reduced.…”

Section: Discussionmentioning

confidence: 82%

“…SIRTs are a highly conserved family of deacetylases, of which the enzymatic activities are strictly regulated by NAD+. 52,53 In LPSinduced DPFs in vitro, we found that the expression of SIRT1 and SIRT6, which are located in the nucleus, was significantly reduced.…”

Section: Silencing Sirt7 Weakens Suppression Of Nf-κb By the Rve1 And...mentioning

confidence: 85%

Combination of resolvin E1 and lipoxin A4 promotes the resolution of pulpitis by inhibiting NF‐κB activation through upregulating sirtuin 7 in dental pulp fibroblasts

et al. 2022

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Objectives: To determine whether the combination of resolvin E1 (RvE1) and lipoxin A4 (LXA4) could promote resolution of pulpitis and to investigate the mechanism. Materials and Methods: Preliminary screening was first conducted in four specialized pro-resolving mediators (SPMs). Real-time quantitative polymerase chain reaction, western blotting, enzyme-linked immunosorbent assay and double-immunofluorescence labelling were employed to assess the expression of RelA, SIRT1, SIRT6, SIRT7 and proinflammatory factors. Dental pulp fibroblasts (DPFs) were transfected with siRNA to assess the biological role of SIRT7. A pulpitis model was utilized to evaluate the in vivo curative effect. Results: Preliminary results showed that RvE1 and LXA4 reduced the expression of RelA more markedly than other two SPMs. Both RvE1 and LXA4 treatment downregulated nuclear factor kappa B (NF-κB) activation and increased the expression of SIRT1, SIRT6 and SIRT7, more so in combination than alone. Double-immunofluorescence labelling showed that SIRT7 co-localized with p-p65 and Ac-p65 in the nucleus. Inhibiting ChemR23 and ALX reversed the expression of RelA mRNA, p-p65 and Ac-p65 proteins, pro-inflammatory factors, SIRT1, SIRT6 and SIRT7. Silencing SIRT7 significantly increased p-p65 and Ac-p65 protein levels and decreased SIRT1 and SIRT6 expression. In vivo experiments showed that combined administration of RvE1 and LXA4 promoted pulpitis markedly to resolution. Conclusions: Combination of RvE1 and LXA4 effectively inhibited NF-κB activation by upregulating SIRT7 expression in DPFs, leading to reduced production of proinflammatory factors and promotion of pulpitis resolution.

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“…Sirtuins (SIRTs, SIRT1-7), ubiquitous deacetylases, are crucial metabolic regulators, and importantly, SIRTs are also emerging as the essential cause of NAFLD ( Nassir and Ibdah, 2016 ; Palomer et al, 2021 ). SIRTs play master roles in a range of physiological functions, including fatty acid oxidation, mitochondrial oxidative metabolism, hepatic fat metabolism, and insulin secretion in hepatocytes ( Nasrin et al, 2010 ; Laurent et al, 2013 ; Gupta et al, 2022 ).…”

Section: Hfd-induced Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

Targeting Gut Microbiota With Natural Polysaccharides: Effective Interventions Against High-Fat Diet-Induced Metabolic Diseases

et al. 2022

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Unhealthy diet, in particular high-fat diet (HFD) intake, can cause the development of several metabolic disorders, including obesity, hyperlipidemia, type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), and metabolic syndrome (MetS). These popular metabolic diseases reduce the quality of life, and induce premature death worldwide. Evidence is accumulating that the gut microbiota is inextricably associated with HFD-induced metabolic disorders, and dietary intervention of gut microbiota is an effective therapeutic strategy for these metabolic dysfunctions. Polysaccharides are polymeric carbohydrate macromolecules and sources of fermentable dietary fiber that exhibit biological activities in the prevention and treatment of HFD-induced metabolic diseases. Of note, natural polysaccharides are among the most potent modulators of the gut microbiota composition. However, the prebiotics-like effects of polysaccharides in treating HFD-induced metabolic diseases remain elusive. In this review, we introduce the critical role of gut microbiota human health and HFD-induced metabolic disorders. Importantly, we review current knowledge about the role of natural polysaccharides in improving HFD-induced metabolic diseases by regulating gut microbiota.

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Sirtuins: To Be or Not To Be in Diabetic Cardiomyopathy

Cited by 28 publications

References 119 publications

Oxidative stress and inflammation regulation of sirtuins: New insights into common oral diseases

Oxidative stress and inflammation regulation of sirtuins: New insights into common oral diseases

Combination of resolvin E1 and lipoxin A4 promotes the resolution of pulpitis by inhibiting NF‐κB activation through upregulating sirtuin 7 in dental pulp fibroblasts

Targeting Gut Microbiota With Natural Polysaccharides: Effective Interventions Against High-Fat Diet-Induced Metabolic Diseases

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