Cellular senescence: when bad things happen to good cells

By J. Campisi, F. d’Adda di Fagagna. Nature reviews. Molecular cell biology, 2007

4,385 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/4b58002a97d8538ca27f439b335e3344b2bd5615

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. M. Demaria
3. Adam Freund
4. F. Rodier
5. D. Meek
6. P. Desprez
7. T. Tchkonia
8. J. Kirkland

In Physiology

1. J. Campisi
2. M. Demaria
3. J. Kirkland
4. Adam Freund
5. T. Tchkonia
6. F. Rodier
7. P. Desprez
8. C. Patil

Citations in the corpus

• The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression (2010, background): “The idea that processes can have such dual effects is consistent with a major evolutionary theory of aging termed antagonistic pleiotropy (19).”
• Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “The senescence program locks the cell into a cell cycle arrest that prevents the damage from affecting the next cell generation, thereby preventing potential malignant transformation [24].”
• Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. (2013, neutral): “Cellular senescence refers to the essentially irreversible growth arrest that occurs when cells experience potentially oncogenic insults (33–38).”
• Protocols to detect senescence-associated beta-galactosidase (SA-βgal) activity, a biomarker of senescent cells in culture and in vivo (2009, background): “Subsequent studies showed that, in addition to the permanent arrest of cell division, senescent cells acquired striking phenotypic changes, including resistance to apoptosis and an altered pattern of gene expressio”
• Cellular senescence drives age-dependent hepatic steatosis (2017, neutral): “Senescent cells frequently have increased secretion of a broad repertoire of proinflammatory factors, collectively known as the senescence-associated secretory phenotype, which can induce tissue dysfunction in a paracrine manner 6 .”
• Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008, background): “Several lines of evidence indicate that cellular senescence is a potent tumor-suppressive mechanism [4,9,10].”