Histone deacetylase 1 expression is inversely correlated with age in the short-lived fish Nothobranchius furzeri

Zupkovitz, Gordin; Lagger, Sabine; Martin, David; Steiner, Marianne; Hagelkrüys, Astrid; Seiser, Christian; Schöfer, Christian; Pusch, Oliver

doi:10.1007/s00418-018-1687-4

Cited by 14 publications

(12 citation statements)

References 55 publications

(84 reference statements)

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“…Another group measured an increase in HDAC2 levels in the mouse hippocampus with aging that was prevented by CR [ 169 ]. In contrast to the hippocampal HDAC2 protein level measurements, whole brain HDAC2 mRNA levels (as well as the levels of HDAC3 and HDAC8) declined with murine aging, while HDAC1 mRNA levels did not change [ 170 ]. In mice from two months to eight months of age, histone acetylation was found to increase in white matter oligodendrocytes due a decrease in class I HDAC activity [ 171 ].…”

Section: Cr Increases Hat and Decreases Hdac Activity In Brain Cortexmentioning

confidence: 99%

Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan

Bradshaw

2021

Antioxidants

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Acetyl-CoA is a metabolite at the crossroads of central metabolism and the substrate of histone acetyltransferases regulating gene expression. In many tissues fasting or lifespan extending calorie restriction (CR) decreases glucose-derived metabolic flux through ATP-citrate lyase (ACLY) to reduce cytoplasmic acetyl-CoA levels to decrease activity of the p300 histone acetyltransferase (HAT) stimulating pro-longevity autophagy. Because of this, compounds that decrease cytoplasmic acetyl-CoA have been described as CR mimetics. But few authors have highlighted the potential longevity promoting roles of nuclear acetyl-CoA. For example, increasing nuclear acetyl-CoA levels increases histone acetylation and administration of class I histone deacetylase (HDAC) inhibitors increases longevity through increased histone acetylation. Therefore, increased nuclear acetyl-CoA likely plays an important role in promoting longevity. Although cytoplasmic acetyl-CoA synthetase 2 (ACSS2) promotes aging by decreasing autophagy in some peripheral tissues, increased glial AMPK activity or neuronal differentiation can stimulate ACSS2 nuclear translocation and chromatin association. ACSS2 nuclear translocation can result in increased activity of CREB binding protein (CBP), p300/CBP-associated factor (PCAF), and other HATs to increase histone acetylation on the promoter of neuroprotective genes including transcription factor EB (TFEB) target genes resulting in increased lysosomal biogenesis and autophagy. Much of what is known regarding acetyl-CoA metabolism and aging has come from pioneering studies with yeast, fruit flies, and nematodes. These studies have identified evolutionary conserved roles for histone acetylation in promoting longevity. Future studies should focus on the role of nuclear acetyl-CoA and histone acetylation in the control of hypothalamic inflammation, an important driver of organismal aging.

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Section: Cr Increases Hat and Decreases Hdac Activity In Brain Cortexmentioning

confidence: 99%

Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan

Bradshaw

2021

Antioxidants

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“…SIRT6 is an important regulator of DNA repair enzymes and a chromatin modifier in response to DNA damage; its reduction plays a critical role in genomic instability [ 58 ]. Class I HDACs also decrease their activity during aging, which is especially pronounced in the brain [ 59 , 60 , 61 ]. These proteins are assembled into the nucleosome remodeling and deacetylation complex (NuRD), which is involved in the regulation of nucleosome position, and histone deacetylase activity and controls DNA damage response [ 60 ].…”

Section: Impairment Of the Mechanisms For Maintaining Genome Stabimentioning

confidence: 99%

Genome-Protecting Compounds as Potential Geroprotectors

Proshkina

Shaposhnikov

Moskalev

2020

IJMS

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Throughout life, organisms are exposed to various exogenous and endogenous factors that cause DNA damages and somatic mutations provoking genomic instability. At a young age, compensatory mechanisms of genome protection are activated to prevent phenotypic and functional changes. However, the increasing stress and age-related deterioration in the functioning of these mechanisms result in damage accumulation, overcoming the functional threshold. This leads to aging and the development of age-related diseases. There are several ways to counteract these changes: (1) prevention of DNA damage through stimulation of antioxidant and detoxification systems, as well as transition metal chelation; (2) regulation of DNA methylation, chromatin structure, non-coding RNA activity and prevention of nuclear architecture alterations; (3) improving DNA damage response and repair; (4) selective removal of damaged non-functional and senescent cells. In the article, we have reviewed data about the effects of various trace elements, vitamins, polyphenols, terpenes, and other phytochemicals, as well as a number of synthetic pharmacological substances in these ways. Most of the compounds demonstrate the geroprotective potential and increase the lifespan in model organisms. However, their genome-protecting effects are non-selective and often are conditioned by hormesis. Consequently, the development of selective drugs targeting genome protection is an advanced direction.

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“…Surely, the epigenome can be influenced by exogenous and endogenous factors ( Pal and Tyler, 2016 ). In the killifish brain, Hdac1 and Hdac3, genes with a function in chromatin remodeling, more specifically histone modification, are significantly downregulated upon aging ( Zupkovitz et al, 2018 ). In addition, the zebrafish brain shows age-related hypomethylation ( Shimoda et al, 2014 ).…”

Section: Evidence For Molecular and Cellular Hallmarks Of Aging In Thmentioning

confidence: 99%

Modeling Neuroregeneration and Neurorepair in an Aging Context: The Power of a Teleost Model

houcke

Mariën

Zandecki

et al. 2021

Front. Cell Dev. Biol.

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Aging increases the risk for neurodegenerative disease and brain trauma, both leading to irreversible and multifaceted deficits that impose a clear societal and economic burden onto the growing world population. Despite tremendous research efforts, there are still no treatments available that can fully restore brain function, which would imply neuroregeneration. In the adult mammalian brain, neuroregeneration is naturally limited, even more so in an aging context. In view of the significant influence of aging on (late-onset) neurological disease, it is a critical factor in future research. This review discusses the use of a non-standard gerontology model, the teleost brain, for studying the impact of aging on neurorepair. Teleost fish share a vertebrate physiology with mammals, including mammalian-like aging, but in contrast to mammals have a high capacity for regeneration. Moreover, access to large mutagenesis screens empowers these teleost species to fill the gap between established invertebrate and rodent models. As such, we here highlight opportunities to decode the factor age in relation to neurorepair, and we propose the use of teleost fish, and in particular killifish, to fuel new research in the neuro-gerontology field.

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Histone deacetylase 1 expression is inversely correlated with age in the short-lived fish Nothobranchius furzeri

Cited by 14 publications

References 55 publications

Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan

Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan

Genome-Protecting Compounds as Potential Geroprotectors

Modeling Neuroregeneration and Neurorepair in an Aging Context: The Power of a Teleost Model

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