Senescence-messaging secretome: SMS-ing cellular stress

By T. Kuilman, D. Peeper. Nature Reviews. Cancer, 2009

892 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/06e558e3ee715e7242940785a9bab0e4853f086b

How researchers see this paper

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

In Molecular Biology

1. J. Campisi
2. Jesús Gil
3. M. Demaria
4. Nicolás Herranz
5. T. Tchkonia
6. J. Kirkland
7. Adam Freund
8. P. Desprez

In Oncology

1. J. Campisi
2. Jesús Gil
3. Manuel Serrano
4. M. Collado
5. Nicolás Herranz
6. M. Demaria
7. Adam Freund
8. Zhijian J. Chen

In Physiology

1. J. Campisi
2. Jesús Gil
3. M. Demaria
4. J. Kirkland
5. Adam Freund
6. T. Tchkonia
7. Manuel Serrano
8. P. Desprez

Citations in the corpus

• Senescence and apoptosis: dueling or complementary cell fates? (2014, positive): “This expectation is especially true in light of the fact that senescent cells actively secrete a suite of cytokines, chemokines, and matrix-remodeling enzymes known as the senescence-associated secretory phenotype (SASP) [25,26] or senescence-messaging secretome (SMS) [27].”
• The senescence-associated secretory phenotype and its physiological and pathological implications (2024, neutral): “In 2008, different laboratories independently described the SASP (or the senescence-messaging secretome) 14–17 , primarily as a collection of pro-inflammatory and growth-stimulating proteins.”
• The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer (2018, background): “How does the cGAS–STI NG pathway regulate cellular senescence, given that it is not an integral component of either the p53–p21 or the p16 INK4a–Rb pathway? A mechanism is likely through the senescence-associated secretory phenotype (SASP), which refers to the phenomenon that senescent cells produce”
• Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “Senescent cells secrete hundreds of factors that include proinflammatory cytokines, chemokines, growth factors, and proteases (Kuilman and Peeper, 2009; Coppé et al., 2010).”
• Cellular senescence drives age-dependent hepatic steatosis (2017, positive): “…senescence markers and genes involved in inflammatory responses was anticipated because senescence entails molecular reprogramming and production of a unique secretome characterized by the increased release of cytokines, chemokines, extracellular matrix remodelling factors and growth factors 23 .”
• Mechanisms and functions of cellular senescence. (2018, neutral): “Senescent cells produce a complex mixture of soluble and insoluble factors that are collectively termed senescence-associated secretory phenotype (SASP) or senescence-messaging secretome (58, 59).”
• mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype (2015, positive): “In contrast, the SASP can induce senescence 4,6,7 and activate the immune system to keep neoplastic cells in check 8 .”