Caloric restriction, resveratrol and melatonin: Role of SIRT1 and implications for aging and related-diseases

Ramis, Margarita; Esteban, Susana; Miralles, Antonio; Tan, Dun Xian; Reíter, Russel J.

doi:10.1016/j.mad.2015.03.008

Cited by 138 publications

(94 citation statements)

References 270 publications

(378 reference statements)

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“…SIRT1 has the capability to extend life span, delay aging, and prevent aging-related diseases, mainly by catalyzing the deacetylation of histones, and regulation of transcription factors, or coactivators, such as p53, forkhead box O (FOXO), nuclear factor-κB (NF-κB), PGC-1α, and Ku70 (Ramis et al, 2015). Although there is no decline in SIRT1 protein with age, SIRT1 activity might be compromised in old mice due to the systemic decline in NAD.…”

Section: What Causes the Nad Decline Observed During The Aging Process?mentioning

confidence: 99%

NAD and the aging process: Role in life, death and everything in between

Chini

Tarragó

Chini

2017

Molecular and Cellular Endocrinology

153

179

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Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide (NAD). From the simplest organism, such as bacteria, to the most complex multicellular organisms, NAD is a key cellular component. NAD is extremely abundant in most living cells and has traditionally been described to be a cofactor in electron transfer during oxidation-reduction reactions. In addition to participating in these reactions, NAD has also been shown to play a key role in cell signaling, regulating several pathways from intracellular calcium transients to the epigenetic status of chromatin. Thus, NAD is a molecule that provides an important link between signaling and metabolism, and serves as a key molecule in cellular metabolic sensoring pathways. Importantly, it has now been clearly demonstrated that cellular NAD levels decline during chronological aging. This decline appears to play a crucial role in the development of metabolic dysfunction and age-related diseases. In this review we will discuss the molecular mechanisms responsible for the decrease in NAD levels during aging. Since other reviews on this subject have been recently published, we will concentrate on presenting a critical appraisal of the current status of the literature and will highlight some controversial topics in the field. In particular, we will discuss the potential role of the NADase CD38 as a driver of age-related NAD decline.

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Section: What Causes the Nad Decline Observed During The Aging Process?mentioning

confidence: 99%

NAD and the aging process: Role in life, death and everything in between

Chini

Tarragó

Chini

2017

Molecular and Cellular Endocrinology

153

179

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“…Chronic kidney disease (CKD): defined by the National Kidney Foundation as a persistent (>3 months) glomerular filtration rate (GFR) of less than 60 ml per minute per 1.73 m 2 of body surface area or the presence of kidney damage, regardless of the cause, and impaired kidney function [1]. Histone deacetylase (HDAC): histone acetylation mediated by histone acetyltransferases promotes an open chromatin formation, which provides binding sites for basal transcription factors and RNA polymerase II to facilitate gene transcription [40]. By contrast, HDACs remove acetyl groups from lysine residues of histones, resulting in chromatin compaction and transcription repression.…”

Section: The Renin-angiotensin System (Ras) In Liver and Kidney Diseasementioning

confidence: 99%

“…The deacetylation of proteins and histones results in an up-or downregulation of gene transcription and protein function, and plays a crucial regulatory role in numerous cellular functions [40]. Recently, the regulatory function of SIRT1 received much attention owing to its calorie restriction-mimicking activity and beneficial effects on obesity-related disorders, including NAFLD and CKD.…”

Section: Role Of Energy and Nutrient Sensors 5 0 -Amp-activated Protmentioning

confidence: 99%

Emerging Liver–Kidney Interactions in Nonalcoholic Fatty Liver Disease

Musso

Cassader

Cohney

et al. 2015

Trends in Molecular Medicine

100

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“…Sirtuins can be activated under certain stress conditions such as starvation and caloric restriction [254][255][256] to increase the efficiency of metabolism to cope with metabolic stress. However, sirtuins are usually less active under overnutrition conditions such as diabetes because of overproduction of NADH that can inhibit sirtuins activity [257,258].…”

Section: Protein Acetylationmentioning

confidence: 99%

Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity

Luo¹,

Wu²,

Si-qun³

et al. 2016

Aging and disease

104

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Diabetes and its complications are caused by chronic glucotoxicity driven by persistent hyperglycemia. In this article, we review the mechanisms of diabetic glucotoxicity by focusing mainly on hyperglycemic stress and carbon stress. Mechanisms of hyperglycemic stress include reductive stress or pseudohypoxic stress caused by redox imbalance between NADH and NAD + driven by activation of both the polyol pathway and poly ADP ribose polymerase; the hexosamine pathway; the advanced glycation end products pathway; the protein kinase C activation pathway; and the enediol formation pathway. Mechanisms of carbon stress include excess production of acetyl-CoA that can over-acetylate a proteome and excess production of fumarate that can over-succinate a proteome; both of which can increase glucotoxicity in diabetes. For hyperglycemia stress, we also discuss the possible role of mitochondrial complex I in diabetes as this complex, in charge of NAD + regeneration, can make more reactive oxygen species (ROS) in the presence of excess NADH. For carbon stress, we also discuss the role of sirtuins in diabetes as they are deacetylases that can reverse protein acetylation thereby attenuating diabetic glucotoxicity and improving glucose metabolism. It is our belief that targeting some of the stress pathways discussed in this article may provide new therapeutic strategies for treatment of diabetes and its complications.

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Caloric restriction, resveratrol and melatonin: Role of SIRT1 and implications for aging and related-diseases

Cited by 138 publications

References 270 publications

NAD and the aging process: Role in life, death and everything in between

NAD and the aging process: Role in life, death and everything in between

Emerging Liver–Kidney Interactions in Nonalcoholic Fatty Liver Disease

Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity

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