2016
DOI: 10.18632/aging.100905
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Abstract: Mammalian sirtuins are involved in the control of metabolism and life-span regulation. Here, we link the mitochondrial sirtuin SIRT4 with cellular senescence, skin aging, and mitochondrial dysfunction. SIRT4 expression significantly increased in human dermal fibroblasts undergoing replicative or stress-induced senescence triggered by UVB or gamma-irradiation. In-vivo, SIRT4 mRNA levels were upregulated in photoaged vs. non-photoaged human skin. Interestingly, in all models of cellular senescence and in photoag… Show more

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Cited by 94 publications
(129 citation statements)
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References 105 publications
(129 reference statements)
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“…In this study, we discovered that SIRT4 protein levels are increased in oocytes from old mouse (Figure 7). Likewise, SIRT4 expression is upregulated during senescence triggered by different stimuli in human skin cells and trophoblast stem cells (Castex et al., 2017; Lang et al., 2016). SIRT4 upregulation has also been implicated to adversely impact mitochondrial functions and contribute to the development of senescent phenotypes (Castex et al., 2017).…”
Section: Discussionmentioning
confidence: 99%
“…In this study, we discovered that SIRT4 protein levels are increased in oocytes from old mouse (Figure 7). Likewise, SIRT4 expression is upregulated during senescence triggered by different stimuli in human skin cells and trophoblast stem cells (Castex et al., 2017; Lang et al., 2016). SIRT4 upregulation has also been implicated to adversely impact mitochondrial functions and contribute to the development of senescent phenotypes (Castex et al., 2017).…”
Section: Discussionmentioning
confidence: 99%
“…In Dicer Δ/Δ CD4 + T cells, the enhanced Nhe1 expression could further result from acidic pHi. According to a recent study, inhibition of miR-15b increases the ROS production, decreases the mitochondrial membrane potential, and modulates mRNA levels of nuclear encoded mitochondrial genes (CytC, TFAM, NRF1) as well as components of the senescence-associated secretory phenotype (IL-6, IL-8, VEGF, MMP1, IL-1-α, IL-1β, and IFN-γ) via Sirtuin4 (SIRT4) [51]. In Dicer Δ/Δ CD4 + T cells, phosphorylation of Akt on both Ser473 and Thr308 after TCR activation is augmented [35].…”
Section: Discussionmentioning
confidence: 99%
“…Likewise, SIRT4 may affect ROS via pyruvate dehydrogenase complex (PDH), glutamate dehydrogenase (GDH) and fatty acid oxidation through malonyl-CoA decarboxylase (MCD) [4850]. While this will ultimately lead to decreased donation of electrons to the ETC and reduce the production of ROS, recent studies suggest that Sirt4 activity may increase ROS levels in murine cardiomyocytes [51,52]. In sum, decline of sirtuin activity during aging may compromise the signaling function of balanced ROS levels to impair mitochondrial and cellular homeostasis.…”
Section: Mitochondrial Sirtuins Protect Against Age-related Diseasesmentioning
confidence: 99%