Sirtuins, aging, and cardiovascular risks

Favero, Gaia; Franceschetti, Lorenzo; Rodella, Luigi Fabrizio

doi:10.1007/s11357-015-9804-y

Cited by 27 publications

(22 citation statements)

References 194 publications

(242 reference statements)

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“…Sirtuins deacetylate histones and nonhistone proteins with equal efficiency (14). Seven types of sirtuins serve as epigenetic transcriptional silencers (7,18). Sirtuins attenuate NF-B signaling via deacetylation of either NF-B subunits or histone proteins at target promoter region (2,17).…”

mentioning

confidence: 99%

Hsp90 inhibition suppresses NF-κB transcriptional activation via Sirt-2 in human lung microvascular endothelial cells

Thangjam

Birmpas

Barabutis

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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mentioning

confidence: 99%

Hsp90 inhibition suppresses NF-κB transcriptional activation via Sirt-2 in human lung microvascular endothelial cells

Thangjam

Birmpas

Barabutis

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…AMPK phosphorylates TSC2 to increase GAP activity to change Rheb-GTP into the inactive Rheb-GDP and to inhibit mTORC1 activity (120). As noted above, AMPK also functions with SIRT1 (13, 62). In addition, AMPK can increase nicotinamide phosphoribosyltransferase (NAMPT) activity to convert nicotinamide to nicotinamide mononucleotide (57, 121, 122).…”

Section: The Mechanistic Target Of Rapamycin (Mtor)mentioning

confidence: 79%

“…Systems of the body may become affected with age-related disorders disorders, such as lung disease and increased inflammation, which can become detrimental to overall lifespan (12). Cardiovascular disease (13, 14), musculoskeletal disease (15, 16), and psychiatric disorders (17) also can progress with aging. Equally important is the impact of aging on the nervous system (18).…”

Section: Increased Lifespan Degenerative Disorders and Cell Injurymentioning

confidence: 99%

“…AMPK activation also may improve memory retention in models of AD and DM (114). With silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae ) (SIRT1) (13, 62), AMPK can protect endothelial cells through the induction of autophagy against oxidized low-density lipoproteins (115). Yet, limited AMPK activity also may be required for cellular protection.…”

Section: The Mechanistic Target Of Rapamycin (Mtor)mentioning

confidence: 99%

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Erythropoietin and mTOR: A “One-Two Punch” for Aging-Related Disorders Accompanied by Enhanced Life Expectancy

Maiese¹

2016

CNR

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Life expectancy continues to increase throughout the world, but is accompanied by a rise in the incidence of non-communicable diseases. As a result, the benefits of an increased lifespan can be limited by aging-related disorders that necessitate new directives for the development of effective and safe treatment modalities. With this objective, the mechanistic target of rapamycin (mTOR), a 289-kDa serine/threonine protein, and its related pathways of mTOR Complex 1 (mTORC1), mTOR Complex 2 (mTORC2), proline rich Akt substrate 40 kDa (PRAS40), AMP activated protein kinase (AMPK), Wnt signaling, and silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), have generated significant excitement for furthering novel therapies applicable to multiple systems of the body. Yet, the biological and clinical outcome of these pathways can be complex especially with oversight of cell death mechanisms that involve apoptosis and autophagy. Growth factors, and in particular erythropoietin (EPO), are one avenue under consideration to implement control over cell death pathways since EPO can offer potential treatment for multiple disease entities and is intimately dependent upon mTOR signaling. In experimental and clinical studies, EPO appears to have significant efficacy in treating several disorders including those involving the developing brain. However, in mature populations that are affected by aging-related disorders, the direction for the use of EPO to treat clinical disease is less clear that may be dependent upon a number of factors including the understanding of mTOR signaling. Continued focus upon the regulatory elements that control EPO and mTOR signaling could generate critical insights for targeting a broad range of clinical maladies.

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“…As a result, new avenues of investigation to develop novel therapies against vascular disease are required to stem this tide of vascular disease. One such avenue involves the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae ) (SIRT1) that is under such consideration for the development of new treatments against vascular disease (29, 35, 41–47). …”

Section: Sirt1 As a Target For Vascular Diseasementioning

confidence: 99%

Harnessing the Power of SIRT1 and Non-coding RNAs in Vascular Disease

Maiese¹

2017

CNR

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Noncommunicable diseases (NCDs) contribute to a significant amount of disability and death in the world. Of these disorders, vascular disease is ranked high, falls within the five leading causes of death, and impacts multiple other disease entities such as those of the cardiac system, nervous system, and metabolic disease. Targeting the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) pathway and the modulation of micro ribonucleic acids (miRNAs) may hold great promise for the development of novel strategies for the treatment of vascular disease since each of these pathways are highly relevant to cardiac and nervous system disorders as well as to metabolic dysfunction. SIRT1 is vital in determining the course of stem cell development and the survival, metabolism, and life span of differentiated cells that are overseen by both autophagy and apoptosis. SIRT1 interfaces with a number of pathways that involve forkhead transcription factors, mechanistic of rapamycin (mTOR), AMP activated protein kinase (AMPK) and Wnt1 inducible signaling pathway protein 1 (WISP1) such that the level of activity of SIRT1 can become a critical determinant for biological and clinical outcomes. The essential fine control of SIRT1 is directly tied to the world of non-coding RNAs that ultimately oversee SIRT1 activity to either extend or end cellular survival. Future studies that can further elucidate the crosstalk between SIRT1 and non-coding RNAs should serve well our ability to harness the power of SIRT1 and non-coding RNAs for the treatment of vascular disorders.

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Sirtuins, aging, and cardiovascular risks

Cited by 27 publications

References 194 publications

Hsp90 inhibition suppresses NF-κB transcriptional activation via Sirt-2 in human lung microvascular endothelial cells

Hsp90 inhibition suppresses NF-κB transcriptional activation via Sirt-2 in human lung microvascular endothelial cells

Erythropoietin and mTOR: A “One-Two Punch” for Aging-Related Disorders Accompanied by Enhanced Life Expectancy

Harnessing the Power of SIRT1 and Non-coding RNAs in Vascular Disease

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