Increased Wnt Signaling During Aging Alters Muscle Stem Cell Fate and Increases Fibrosis
By A. Brack, M. Conboy, Sudeep Roy, Mark Lee, C. Kuo, C. Keller, T. Rando. Science, 2007
1,519 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/791528918c12c0702ddbaf4667384918b34f3a70
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In Genetics
- S. Morrison
- Irving L. Weissman
- R. DePinho
- Catriona H. M. Jamieson
- Derrick J. Rossi
- Michael A. Rudnicki
- William C. Hahn
- Austin G Smith
In Molecular Biology
- S. Morrison
- Irving L. Weissman
- Derrick J. Rossi
- R. DePinho
- D. Sinclair
- Shenghui He
- Catriona H. M. Jamieson
- Daisuke Nakada
Citations in the corpus
- The aged niche disrupts muscle stem cell quiescence (2012, background): “The young systemic environment stimulates SC proliferation; the aged systemic environment inhibits SC proliferation 9,12 .”
- The SIRT1 Deacetylase Suppresses Intestinal Tumorigenesis and Colon Cancer Growth (2008, background): “Interestingly, two recent studies have shown that increased Wnt signaling is associated with accelerated aging, suggesting that an attenuation of Wnt signaling might underlie CR and be beneficial not only for treating cancer but for more broadly attenuating diseases of aging [23,24].”
- Aberrant repair and fibrosis development in skeletal muscle (2011, background): “An earlier study by the same group had already highlighted the role of the canonical Wnt pathway in ageassociated fibrosis, linking increased collagen deposition in aged regenerating muscles to a greater percentage of fibrogenic cells arising from the conversion of myogenic into non-myogenic cells [”
- Functionally distinct hematopoietic stem cells modulate hematopoietic lineage potential during aging by a mechanism of clonal expansion (2010, background): “However, as the epigenetic marks underlying these changes may be quite stable, it remains possible that ageassociated changes inHSC lineage potential may still be guided by instructive signals emanating from the aged systemic or microenvironments, as is the case with other stem cell systems (20, 21)”
- FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis (2009, background): “Furthermore, consistent with a possible role of elevated Wnt signaling in stem cell maintenance, addition of Wnt has been shown to convert myogenic progenitor culture into fibrogenic lineage (Brack et al., 2007).”
- Fibrosis and adipogenesis originate from a common mesenchymal progenitor in skeletal muscle (2011, background): “Brack and colleagues also reported that myogenic cells become fibroblastic cells during aging in response to increased Wnt signaling (Brack et al., 2007).”
- Growth Differentiation Factor 11 is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy (2013, neutral): “Conversely, exposing a young mouse to an old systemic environment can inhibit myogenesis (Brack et al., 2007) and neurogenesis (Villeda et al., 2011) in the young mouse.”
- Mechanisms of stem cell self-renewal. (2009, background): “It appears that such circulating factors include Wnts, because canonical Wnt pathway activation increases with age in muscle satellite cells, and inhibitors of this pathway can restore myogenesis by satellite cells (Brack et al. 2007).”
- Satellite cells and the muscle stem cell niche. (2013, background): “Increased levels of fat and connective tissue (fibrosis), evidence for increased numbers of adipocytes and fibroblasts, respectively, are well documented for several physiological and pathological conditions, such as aging, obesity, and muscular dystrophy (38, 66, 195, 198, 200).”
- Stems cells and the pathways to aging and cancer. (2008, background): “, 2006) and the tendency of satellite cells to convert from their normal myogenic fate to a fibrotic fate with age due to elevated Wnt signaling originating from the serum of old mice (Brack et al., 2007).”