The essence of senescence.
By T. Kuilman, C. Michaloglou, W. Mooi, D. Peeper. Genes & Development, 2010
2,102 citations recorded by the source corpus.
Almost half a century after the first reports describing the limited replicative potential of primary cells in culture, there is now overwhelming evidence for the existence of "cellular senescence" in vivo. It is being recognized as a critical feature of mammalian cells to suppress tumorigenesis, acting alongside cell death programs. Here, we review the various features of cellular senescence and discuss their contribution to tumor suppression. Additionally, we highlight the power and limitations of the biomarkers currently used to identify senescent cells in vitro and in vivo.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/929721c759b451cbbf8b6970f5013982b80d968d
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In Molecular Biology
- J. Campisi
- Jesús Gil
- M. Demaria
- Adam Freund
- Manuel Serrano
- Guido Kroemer
- Domhnall McHugh
- Linda Partridge
In Physiology
- J. Campisi
- Jesús Gil
- M. Demaria
- Manuel Serrano
- Adam Freund
- Domhnall McHugh
- Guido Kroemer
- Rémi-Martin Laberge
Citations in the corpus
- cGAS is essential for cellular senescence (2017, background): “Senescence is characterized by several unique features, including enlarged and flattened cell morphology (5), increased senescence-associated β-galactosidase (SA-β-Gal) activity (6, 7), and in some cell types, a widespread change in chromatin modification, known as senescence-associated heterochroma”
- Cellular senescence and its effector programs (2014, background): “Thus, more generally, senescence can be described as a state of stable cell cycle arrest in response to diverse stresses (Campisi and d’Adda di Fagagna 2007; Collado et al. 2007; Kuilman et al. 2010).”
- Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases. (2018, background): “induced by various stimuli and characterized by chromatin remodeling, endoplasmic reticulum stress, and increased β-galactosidase activity and autophagy [260].”
- Mechanisms and functions of cellular senescence. (2018, neutral): “Currently, senescence is considered a stress response that can be induced by a wide range of intrinsic and extrinsic insults, including oncogenic activation, oxidative and genotoxic stress, mitochondrial dysfunction, irradiation, or chemotherapeutic agents (3).”
- Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “What is senescence? Senescence is cellular program that induces a stable growth arrest accompanied by distinct phenotypic alterations, including chromatin remodeling, metabolic reprogramming, increased autophagy, and the implementation of a complex proinflammatory secretome (Kuilman et al., 2010; Sa”
- ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age-Related Diseases (2016, background): “Senescent cells proliferate in aging, as a stress response primed by a number of “countingmechanisms,” like telomeres shortening, DNA damage accumulation, abnormal oncogenes activities, metabolic alterations, and excessive ROS generation [7].”
- Senescence is a developmental mechanism that contributes to embryonic growth and patterning. (2013, background): “C Primarily, they are nonproliferating, exhibit activation of senescence-associated beta-galactosidase (SAb-gal) activity, and have enhanced expression of hallmark regulatory proteins (Dimri et al., 1995; Kuilman et al., 2010).”