Tag: sirtuins

Emerging Anti-Aging Strategies – Scientific Basis and Efficacy

This comprehensive review examines the scientific foundations and efficacy of emerging anti-aging strategies aimed at promoting healthier aging and mitigating age-related diseases. Key interventions discussed include caloric restriction, intermittent fasting, senolytics, sirtuin-activating compounds, NAD+ precursors, and stem cell therapies. The review highlights the mechanisms by which these strategies influence aging

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Melatonin and brain inflammaging

This 2015 review explores melatonin’s multifaceted role in mitigating brain inflammaging—a chronic, low-grade inflammation contributing to aging and neurodegeneration. Melatonin functions as a direct and indirect antioxidant, modulates mitochondrial function, and suppresses proinflammatory pathways by inhibiting NADPH oxidase, inducible nitric oxide synthase, and proinflammatory cytokines. It also enhances circadian rhythm

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It Takes Two to Tango: NAD⁺ and Sirtuins in Aging/Longevity Control

This 2016 review elucidates the synergistic relationship between NAD⁺ and sirtuins in regulating aging and longevity. It details how NAD⁺-dependent sirtuins, particularly SIRT1 and SIRT3, influence metabolic pathways, mitochondrial function, and stress responses. The paper discusses how declining NAD⁺ levels with age impair sirtuin activity, leading to disrupted nuclear-mitochondrial communication

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NAD⁺ Repletion Reverses Heart Failure With Preserved Ejection Fraction

This 2021 study demonstrates that NAD⁺ repletion can reverse heart failure with preserved ejection fraction (HFpEF) in a mouse model. Researchers found that HFpEF is associated with reduced myocardial NAD⁺ levels, leading to mitochondrial protein hyperacetylation and impaired fatty acid oxidation. Supplementation with NAD⁺ precursors, such as nicotinamide riboside (NR)

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The Sirtuins, Oxidative Stress and Aging: An Emerging Link

This review explores the role of sirtuins, a family of NAD⁺-dependent deacetylases, in modulating oxidative stress and aging. Sirtuins, particularly SIRT1 and SIRT3, enhance cellular resistance to oxidative damage by deacetylating key transcription factors and enzymes involved in antioxidant defense, such as FOXO proteins and SOD2. Caloric restriction activates sirtuins,

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The multifaceted functions of sirtuins in cancer

This 2015 review explores the diverse roles of sirtuins (SIRT1–SIRT7), a family of NAD⁺-dependent enzymes, in cancer biology. Sirtuins influence key processes such as metabolism, DNA repair, chromatin remodeling, and the tumor microenvironment. For instance, SIRT6 acts as a co-repressor for HIF1α, MYC, and NF-κB, thereby regulating cancer metabolism and

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Pharmacology and Potential Implications of Nicotinamide Adenine Dinucleotide Precursors

This 2021 review examines the pharmacological properties and therapeutic potential of NAD⁺ precursors, including nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), and nicotinic acid (NA). The authors discuss how these compounds enhance NAD⁺ levels, influencing cellular redox states, energy metabolism, and sirtuin activity. The review highlights the role of NAD⁺ in

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NAD⁺ in Brain Aging and Neurodegenerative Disorders

This 2019 review highlights the central role of NAD⁺ in neuronal health, emphasizing its involvement in energy metabolism, DNA repair, mitochondrial function, and stress responses. The authors discuss how declining NAD⁺ levels with age contribute to neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Huntington’s, and ALS. NAD⁺-dependent enzymes, including sirtuins and

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Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs

This 2017 review discusses the roles of resveratrol (RES), curcumin (CUR), and berberine (BBR) in modulating aging, cancer progression, cancer stem cells (CSCs), and microRNA (miR) expression. RES activates sirtuins (e.g., SIRT1), influencing aging and cancer-related pathways. CUR exhibits anti-inflammatory and anti-cancer properties, particularly against CSCs, by affecting gene methylation

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