A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis
By L. Niedernhofer, G. Garinis, A. Raams, A. Lalai, A. Robinson, E. Appeldoorn, H. Odijk, R. Oostendorp, Anwaar Ahmad, W. V. Leeuwen and 8 more. Nature, 2006
685 citations recorded by the source corpus.
Subfields: Aging, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/1dd5633ec93a9287cf961a5601c694eb7c2496ae
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Citations in the corpus
- DNA damage-induced alterations in chromatin contribute to genomic integrity and age-related changes in gene expression (2008, positive): “Transcriptional changes may be a beneficial defense response to cellular damage (Niedernhofer et al., 2006).”
- The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer (2018, background): “Mice lacking ERCC1 display increased genome instability and chronic expression of inflammatory cytokines, leading to premature aging and early death (Melton et al., 1998; Niedernhofer et al., 2006; Karakasilioti et al., 2013).”
- Cellular senescence in cancer and aging. (2007, neutral): “, 2000); similarly, some age prematurely (e.g., ERCC1 null mice; Niedernhofer et al., 2006), whereas others do not; and, finally, the two phenotypes may or may not go together and may or may not correlate with premature cell senescence (reviewed in Lombard et al.”
- Fisetin is a senotherapeutic that extends health and lifespan (2018, background): “These cells undergo premature senescence if grown at atmospheric oxygen [56].”