2018
DOI: 10.18632/aging.101463
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Abstract: Cellular senescence is a complex cell fate response that is thought to underlie several age-related pathologies. Despite a loss of proliferative potential, senescent cells are metabolically active and produce energy-consuming effectors, including senescence-associated secretory phenotypes (SASPs). Mitochondria play crucial roles in energy production and cellular signaling, but the key features of mitochondrial physiology and particularly of mitochondria-derived peptides (MDPs), remain underexplored in senescen… Show more

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Cited by 102 publications
(78 citation statements)
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References 60 publications
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“…We observed increased p21 expression, IL-6 production, cytoplasmic SA-β-Gal and pp53 following H 2 0 2 exposure, which are all recognized characteristics of senescent cells (42). Increased mitochondrial respiration was also a feature of H 2 O 2 treated fibroblasts, a characteristic previously described as being a feature of fibroblasts undergoing replicative senescence (37,38).…”
Section: Discussionsupporting
confidence: 68%
See 1 more Smart Citation
“…We observed increased p21 expression, IL-6 production, cytoplasmic SA-β-Gal and pp53 following H 2 0 2 exposure, which are all recognized characteristics of senescent cells (42). Increased mitochondrial respiration was also a feature of H 2 O 2 treated fibroblasts, a characteristic previously described as being a feature of fibroblasts undergoing replicative senescence (37,38).…”
Section: Discussionsupporting
confidence: 68%
“…To further confirm senescence induction we analysed several mitochondrial characteristics as senescent fibroblasts have previously been reported to have higher levels of mitochondrial respiration (37,38). Accordingly, we tested the mitochondrial function of stress-induced senescent lung fibroblasts.…”
Section: Mitochondrial Perturbations Under Oxidant Induced Senescencementioning
confidence: 99%
“…Though an array of senescence markers has been proposed and widely used in multiple cell types, no single one can reliably identify senescent cells either in vitro or in vivo. The most widely used markers of senescence include the senescence-associated β-galactosidase (SA-β-gal) reactivity [15,20,[35][36][37][38][39], increased expression of the cyclin-dependent kinase (CDK) inhibitor p16INK4a [15,30,[36][37][38][39][40], p21 (CIP1/WAF1) [36-39, 41, 42], p53 [36,37,41,42], induction of SASP factors [14,41,[43][44][45][46][47][48][49][50], mitochondrial DNA modifications [39,[50][51][52][53][54][55][56][57], and chromatin modifications [37,47,58,59] ( Figure 1). The limitation is that even a combination of multiple markers does not truly represent senescence but could also describe long-term cell arrest.…”
Section: Biomarkers Of Senescencementioning
confidence: 99%
“…Repeated exposure stress can also induce ROS which in turn can induce and regulate cellular senescence and can cause major changes in the metabolome [166]. In particular, an increase in mitochondrial oxygen consumption and oxidative phosphorylation have been reported in oncogene-induced senescence in human fibroblasts [166,167], oxidative stress-induced senescence [50,168], therapy-induced senescence in lymphoma [169], and DNA damage-induced senescence [50]. However, in replicative senescence, an impairment of mitochondrial function and increased glycolysis has been described [50,170].…”
Section: Energy Metabolism and Cellular Senescencementioning
confidence: 99%
“…La senescencia celular tendría tanto efectos benéficos como perjudiciales dependiendo del contexto (66), teniendo un papel con-trovertido en el desarrollo del cáncer (67). Entre las desventajas, el fenotipo secretor asociado a la senescencia (SASP) puede perturbar el microambiente, alterar la estructura y el funcionamiento de los tejidos normales, y promover fenotipos malignos en células cercanas.…”
Section: Hn Y Cáncerunclassified