Accumulation of senescent cells in mitotic tissue of aging primates.

By Jessie C. Jeyapalan, Mark Ferreira, John M. Sedivy, U. Herbig. Mechanisms of Ageing and Development, 2007

599 citations recorded by the source corpus.

Subfields: Aging, Dermatology, Physiology

View Paper: https://www.semanticscholar.org/paper/b557dc61ac7d50f5232c2442a9f892aec8fce9c5

How researchers see this paper

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

In Aging

1. J. Kirkland
2. T. Tchkonia
3. M. Demaria
4. D. Peeper
5. T. Kuilman
6. J. Campisi
7. P. Desprez
8. W. Mooi

In Dermatology

1. J. Campisi
2. Masashi Narita
3. Rafik Amir Salama
4. M. Hoare
5. Mahito Sadaie
6. P. Desprez
7. D. Peeper
8. T. Kuilman

In Physiology

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

Citations in the corpus

• Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “Various markers of senescence, including SA- -gal, p16, and DDR, accumulate in tissues of aged mammals including rodents (42, 189, 335), baboons (156, 168), and humans (67, 97, 211, 225, 267), suggesting that senescent cells CELLULAR SENESCENCE”
• The essence of senescence. (2010, background): “In line with the idea that replicative senescence results from telomeric attrition upon prolonged proliferation, senescence is detected mainly in tissues experiencing substantial cellular turnover (Jeyapalan et al. 2007).”
• Four faces of cellular senescence (2011, unknown): “First, senescent cells increase with age in a variety of mammalian tissues (Dimri et al., 1995; Paradis et al., 2001; Melk et al., 2003; Erusalimsky and Kurz, 2005; Jeyapalan et al., 2007; Wang et al., 2009).”
• Cellular senescence: when bad things happen to good cells (2007, background): “In rodents, primates and humans, senescent cells are found in many renewable tissues, including the vasculature, haematopoietic system, many epithelial organs and the strom”
• Lamin B1 loss is a senescence-associated biomarker (2012, background): “These studies have been aided by biomarkers such as SA-βgal activity, expression of the tumor suppressor protein p16, and characteristic DNA damage foci (Dimri et al., 1995; Krishnamurthy et al., 2004; Jeyapalan et al., 2007).”
• Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “Consistent with a role in aging, senescent cells accumulate with age in many rodent, non-human primate, and human tissues [14, 15].”
• Cellular senescence and its effector programs (2014, background): “Indeed, senescent markers, including SA-b-Gal, DDR, telomere dysfunction, and p16, have been detected in various tissues from old individuals (Dimri et al. 1995; Krishnamurthy et al. 2004; Herbig et al. 2006; Jeyapalan et al. 2007; Flores et al. 2008) and agerelated diseased organs in mammals (Minam”
• Telomeres and aging. (2008, background): “However, it has become clear that telomeres are directly responsible for sustained DNA damage signals in senescent cells (54, 203), and DNA damage foci originating from telomeres in senescent cells can readily be detected in vivo (104).”
• Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008, background): “Although some aged tissues contain less than one or only a few percent of senescent cells [29,66,71], others can accumulate as many as 15% senescent cells [65,72].”
• JAK inhibition alleviates the cellular senescence-associated secretory phenotype and frailty in old age (2015, background): “Senescent cells accumulate with aging in the skin (13, 14), liver (15, 16), kidney (17), the cardiovascular system (18), and other tissues in various species (16).”
• DNA damage response and cellular senescence in tissues of aging mice (2009, background): “3A) of skin have repeatedly been related to cellular senescence in dermis and epidermis (Dimri et al., 1995; Herbig et al., 2006; Jeyapalan et al., 2007).”
• p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype (2011, background): “Thus, senescent cells, which increase with age in vivo (Dimri et al, 1995; Paradis et al, 2001; Jeyapalan et al, 2007; Zhou et al, 2008), may contribute to the low-level chronic inflammation that is a hallmark of aged mammalian tissues and many age-related diseases (Freund et al, 2010; Coppe et al,…”