Four faces of cellular senescence

By F. Rodier, J. Campisi. Journal of Cell Biology, 2011

1,978 citations recorded by the source corpus.

Cellular senescence is an important mechanism for preventing the proliferation of potential cancer cells. Recently, however, it has become apparent that this process entails more than a simple cessation of cell growth. In addition to suppressing tumorigenesis, cellular senescence might also promote tissue repair and fuel inflammation associated with aging and cancer progression. Thus, cellular senescence might participate in four complex biological processes (tumor suppression, tumor promotion, aging, and tissue repair), some of which have apparently opposing effects. The challenge now is to understand the senescence response well enough to harness its benefits while suppressing its drawbacks.

Subfields: Immunology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/b832639bfaf1a24117d61ebbd89a4ac788f6a016

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. J. Kirkland
2. T. Tchkonia
3. J. Campisi
4. M. Demaria
5. Adam Freund
6. Claudio Franceschi
7. J. V. van Deursen
8. P. Scherer

In Molecular Biology

1. M. Demaria
2. J. Campisi
3. Adam Freund
4. T. Tchkonia
5. Manuel Serrano
6. J. Kirkland
7. Claudio Franceschi
8. J. V. van Deursen

In Physiology

1. J. Campisi
2. M. Demaria
3. J. Kirkland
4. T. Tchkonia
5. Manuel Serrano
6. Adam Freund
7. Guido Kroemer
8. M. Blasco

Citations in the corpus

• Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. (2013, positive): “The SASP can cause local and potentially systemic inflammation, disrupt tissue architecture, and stimulate growth of nearby malignant cells when the SASP is both pronounced or persistent, as in old age, massive obesity, or pro-gerias (65, 84–88).”
• Wound repair and regeneration: Mechanisms, signaling, and translation (2014, neutral): “3), although there is controversy as to the mechanism (53).”
• Exosomes maintain cellular homeostasis by excreting harmful DNA from cells (2017, positive): “Most noteworthy, however, is the increased secretion of various secretory proteins, such as inflammatory cytokines, chemokines, growth factors and matrix metalloproteinases, into the surrounding extracellular fluid 7–10 .”
• TGF-β1 Signaling and Tissue Fibrosis. (2018, background): “…involucrin and the cyclindependent kinase inhibitor p21Cip1 are suggestive of a senescent phenotype, a phenotype known to be promoted by stress and accompanied by release of pro-inflammatory cytokines, although this possibility has not been directly addressed in the lung (Rodier and Campisi 2011).”
• Measuring biological aging in humans: A quest (2019, background): “…biomarkers described above, including p53, p21, senescence-associated β-galactosidase, and SASP factors, are specific to senescence, and p16Ink4a is not always present (Biran et al., 2017; Haferkamp et al., 2009; Laberge et al., 2012; Noren Hooten & Evans, 2017; Rodier & Campisi, 2011).”
• Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. (2014, background): “several possible mechanisms of chronic inflammation: (i) persistent production of reactive molecules by infiltrating leukocytes designed to kill pathogens, eventually damages the structural and cellular elements of tissues; (ii) damaged nonimmune cells and activated immune cells lead to the producti”
• Foxo3 circular RNA promotes cardiac senescence by modulating multiple factors associated with stress and senescence responses (2016, background): “Cellular senescence, also known as replicative senescence, is characterized by halted mitosis of diploid cells, while organismal senescence is characterized by a reduced stress response and increased homeostatic imbalance, resulting in a loss of normal functions to the organisms.(2) Cellular senesce”
• The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017, positive): “Division-competent cells can also be pushed to senescence though damaging stresses such has oncogene induction, oxidative stress, and double-strand DNA breaks (99).”
• The hallmarks of aging. (2013, background): “…been appreciated that senescent cells manifest dramatic alterations in their secretome, which is particularly enriched in proinflammatory cytokines and matrix metalloproteinases and is referred to as the ‘‘senescence-associated secretory phenotype’’ (Kuilman et al., 2010; Rodier and Campisi, 2011).”
• Lamin B1 loss is a senescence-associated biomarker (2012, background): “Cells were then fixed and average intensity for each condition was calculated. p16INK4A mRNA is increased in vivo after irradiation.”