Cargando…
Insulin Receptor deletion in S100a4-lineage cells accelerates age-related bone loss
Type I and Type II Diabetes dramatically impair skeletal health. Altered Insulin Receptor (IR) signaling is a common feature of both diseases, and insulin has potent bone anabolic functions. Several previous studies have demonstrated that loss of IR in bone cells results in disrupted bone homeostasi...
Autores principales: | Studentsova, Valentina, Knapp, Emma, Loiselle, Alayna E. |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6374520/ https://www.ncbi.nlm.nih.gov/pubmed/30805422 http://dx.doi.org/10.1016/j.bonr.2019.100197 |
Ejemplares similares
-
Cell non-autonomous functions of S100a4 drive fibrotic tendon healing
por: Ackerman, Jessica E, et al.
Publicado: (2019) -
Deletion of EP4 in S100a4-lineage cells reduces scar tissue formation during early but not later stages of tendon healing
por: Ackerman, Jessica E., et al.
Publicado: (2017) -
Scleraxis-lineage cells are required for tendon homeostasis and their depletion induces an accelerated extracellular matrix aging phenotype
por: Korcari, Antonion, et al.
Publicado: (2023) -
Obesity/Type II Diabetes Promotes Function-limiting Changes in Murine Tendons that are not reversed by Restoring Normal Metabolic Function
por: Studentsova, Valentina, et al.
Publicado: (2018) -
Deletion of NFKB1 enhances canonical NF-κB signaling and increases macrophage and myofibroblast content during tendon healing
por: Best, Katherine T., et al.
Publicado: (2019)