Reactive oxygen species act through p38 MAPK to limit the lifespan of hematopoietic stem cells

By Keisuke Ito, A. Hirao, F. Arai, K. Takubo, S. Matsuoka, K. Miyamoto, M. Ohmura, K. Naka, Kentaro Hosokawa, Y. Ikeda and 1 more. Nature Medicine, 2006

1,370 citations recorded by the source corpus.

Subfields: Hematology, Immunology

View Paper: https://www.semanticscholar.org/paper/1a081bf478f2a1e87ef461991a4ee25ea44c4646

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Citations in the corpus

Oxidative stress, DNA methylation and carcinogenesis. (2008, background): “In terms of cell proliferation, ROS have been shown to modulate cell cycle regulation through modulation of various cell cycle proteins including p53 [10] and ATM (ataxia telangiectasia mutated) [11].”
FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress. (2007, background): “…balance between hematopoietic stem cell (HSC) self-renewal and differentiation is not fully understood, though recent studies underscore the importance of cell cycle, apoptosis, and oxidative stress response (reviewed in Attar and Scadden, 2004; Ito et al., 2004, 2006; Passegue et al., 2005).”
Deconstructing stem cell self-renewal: genetic insights into cell-cycle regulation (2008, background): “The expression of p16 is relatively low in the HSCs of young mice and is upregulated with ageing or in response to cellular stresses, including BMT and RO”
BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells (2013, background): “A critical feature of both normal and leukemia primitive populations is quiescence, as increased proliferation can lead to exhaustion of stem cell function (Ito et al., 2006; Tothova et al., 2007).”
Regulation of the INK4b–ARF–INK4a tumour suppressor locus: all for one or one for all (2006, background): “Although there are as yet no details of how this might be achieved, it has the appeal that the p38 pathway can be activated by several stresses that are known to promote senescence, and that inhibitors of p38 signalling can mitigate or delay senescence in various context”
Cellular senescence in cancer and aging. (2007, positive): “It has been recently observed in hematopoietic stem cells that reactive oxygen species activate the expression of the INK4a/ARF locus through p38MAPK, and this limits the functionality of these stem cells (Ito et al., 2006).”
Metabolic Control of Longevity. (2016, background): “Accordingly, treatment with the antioxidant N-acetyl-L-cysteine enhances the replicative potential of mouse HSCs in serial transplantation experiments (Ito et al., 2006).”
The regulation of INK4/ARF in cancer and aging. (2006, positive): “Oxidative stress has also been suggested to induce an Ink4a/Arf-depend- ent decline in HSC function (Ito et al., 2004, 2006).”
Mechanisms of stem cell self-renewal. (2009, background): “Atm-deficient HSCs are depleted due to their accumulation of ROS, which activates p38 MAPK and induces p16Ink4a (Ito et al. 2004, 2006).”