Cellular senescence and its effector programs

By Rafik Amir Salama, Mahito Sadaie, M. Hoare, Masashi Narita. Genes & Development, 2014

801 citations recorded by the source corpus.

Cellular senescence can be described as a state of stable cell cycle arrest in response to diverse stresses. Senescence is a collective phenotype of multiple effectors, and their intensity and combination can be different depending on triggers and cell types. In this review, Salama et al. summarize effector mechanisms and highlight some key components of the collective phenotype of senescence.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/526862fa78494f67e68de937f548ea0298fa8b0e

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In Molecular Biology

1. Jesús Gil
2. J. Campisi
3. M. Demaria
4. Domhnall McHugh
5. Manuel Serrano
6. P. Jat
7. R. Kumari
8. Masashi Narita

In Physiology

1. J. Campisi
2. Jesús Gil
3. M. Demaria
4. Manuel Serrano
5. Domhnall McHugh
6. P. Jat
7. R. Kumari
8. M. Collado

Citations in the corpus

• Cellular Senescence: Defining a Path Forward. (2019, positive): “The normally repressed LINE-1 (L1) retrotransposons are activated, stimulating the cGAS-STING pathway that elicits a type 1 interferon response (see Secretion) (De Cecco et al., 2013).”
• LINE-1 derepression in senescent cells triggers interferon and inflammaging (2019, positive): “Cellular senescence proceeds through an early DNA damage response phase followed by the SASP response 10 .”
• Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021, background): “…of senescent cells is increased lysosomal activity (Kurz et al., 2000; Lee et al., 2006), macromolecular damage (Gorgoulis et al., 2019), and a temporal cascade in the development of the complex senescence-associated secretory phenotype (SASP) (Coppé et al., 2008, 2010a; Saleh et al., 2018).”
• Mechanisms and functions of cellular senescence. (2018, neutral): “These foci can be identified by DAPI staining and are characterized by enrichment of repressive marks such trimethylated H3K9 and heterochromatic protein 1 (HP1), accumulation of high-mobility group HMGA proteins, and loss of linker histone H1 (4).”
• 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”