Increased Wnt Signaling During Aging Alters Muscle Stem Cell Fate and Increases Fibrosis
The University of Texas at San Antonio Health Science Center · VA Palo Alto Health Care System · +2 more institutions
Abstract
The regenerative potential of skeletal muscle declines with age, and this impairment is associated with an increase in tissue fibrosis. We show that muscle stem cells (satellite cells) from aged mice tend to convert from a myogenic to a fibrogenic lineage as they begin to proliferate and that this conversion is mediated by factors in the systemic environment of the old animals. We also show that this lineage conversion is associated with an activation of the canonical Wnt signaling pathway in aged myogenic progenitors and can be suppressed by Wnt inhibitors. Furthermore, components of serum from aged mice that bind to the Frizzled family of proteins, which are Wnt receptors, may account for the elevated Wnt…
Citation impact
- FWCI
- 24.76
- Percentile
- 100%
- References
- 17
Authors
7- ASAndrew S. Brack
The University of Texas at San Antonio Health Science Center, VA Palo Alto Health Care System, Geriatric Research Education and Clinical Center, Stanford University
- MJMichael J. Conboy
The University of Texas at San Antonio Health Science Center, VA Palo Alto Health Care System, Geriatric Research Education and Clinical Center, Stanford University
- SRSudeep Roy
The University of Texas at San Antonio Health Science Center, VA Palo Alto Health Care System, Geriatric Research Education and Clinical Center, Stanford University
- MLMark Lee
The University of Texas at San Antonio Health Science Center, VA Palo Alto Health Care System, Geriatric Research Education and Clinical Center, Stanford University
- CJCalvin J. Kuo
The University of Texas at San Antonio Health Science Center, VA Palo Alto Health Care System, Geriatric Research Education and Clinical Center, Stanford University
Topics & keywords
- Wnt signaling pathway
- Frizzled
- Stem cell
- Cell biology
- Biology
- LRP6
- Fibrosis
- Progenitor cell