Cellular Senescence in Aging Primates

By U. Herbig, Mark Ferreira, Laura Condel, D. Carey, John M. Sedivy. Science, 2006

1,048 citations recorded by the source corpus.

Subfields: Aging, Dermatology, Physiology

View Paper: https://www.semanticscholar.org/paper/128d6dc96eced80012ad6f47817ca94ff1415739

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. Campisi
2. J. Kirkland
3. T. Tchkonia
4. M. Demaria
5. Mark Ferreira
6. D. Peeper
7. T. Kuilman
8. P. Monaghan

In Dermatology

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

In Physiology

1. J. Campisi
2. J. Kirkland
3. T. Tchkonia
4. M. Demaria
5. Adam Freund
6. C. Patil
7. F. Rodier
8. Jean-Philippe Coppé

Citations in the corpus

• Cellular senescence and its effector programs (2014, background): “Persistent DDR in particular, which is represented by telomere dysfunction-induced foci (TIF) (Takai et al. 2003; Herbig et al. 2006) and DNA segments with chromatin alterations reinforcing senescence (DNA-SCAR) (Rodier et al. 2011), has been associated with the maintenance of senescence primarily t”
• The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs (2015, background): “…percent of nucleated cells in very old primates, senescent cells can secrete pro-inflammatory cytokines, chemokines, and extracellular matrix proteases, which together constitute the senescence-associated secretory phenotype or SASP (Herbig et al., 2006; Copp e et al., 2008; Kuilman et al., 2008).”
• An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “However, a recent study indicated that cellular markers of senescence, such as telomere shortening, are exponentially increased with age in skin fibroblasts of primates (100).”
• Age‐related intrinsic changes in human bone‐marrow‐derived mesenchymal stem cells and their differentiation to osteoblasts (2008, background): “There is controversy to what degree such in vitro changes recapitulate organismal aging (Bird et al., 2003; Herbig et al., 2006).”
• DNA damage-induced alterations in chromatin contribute to genomic integrity and age-related changes in gene expression (2008, neutral): “The ‘‘heterochromatin island hypothesis’’ and related hypotheses propose that alterations in chromatin and the resulting gene expression changes can drive the aging process, but evidence is lacking (Cutler, 1995; Imai and Kitano, 1998; Vijg, 2004; Villeponteau, 1997).”
• DNA damage response and cellular senescence in tissues of aging mice (2009, background): “The increase in the frequency of foci-positive dermal fibroblasts with age in mice is significant, but less exaggerated than in the skin of baboons (Herbig et al., 2006; Jeyapalan et al., 2007), possibly because telomere-dependent senescence might be less relevant in wild-type mice with long…”