JAK-STAT and bone metabolism

@article{Li2013JAKSTATAB,
  title={JAK-STAT and bone metabolism},
  author={Jiliang Li},
  journal={JAK-STAT},
  year={2013},
  volume={2}
}
Emerging evidences suggest Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway plays an important role in bone development and metabolism. Effects of JAK-STAT pathway on skeletal development are summarized based on skeletal phenotype of individual JAK and STAT gene knockout mouse. Furthermore, STAT3 has more profound effects on bone homeostasis compared with the other STATs. STAT3 mutation causes a disease called Job syndrome, most patients with which… 
JAK/STAT Activation: A General Mechanism for Bone Development, Homeostasis, and Regeneration
TLDR
The role of JAK/STAT pathway on development, homeostasis, and regeneration is summarized based on skeletal phenotype of individual JAK and STAT gene knockout models and selective inhibition of components of the Jak/STAT signaling including influences of Jak inhibition in osteoclasts, osteoblasts, and osteocytes.
JAK/STAT pathway and molecular mechanism in bone remodeling
TLDR
The aim, through careful research in literature, has been to provide an overview of the role of the JAK/STAT pathway in bone remodeling and on bone cells, with a focus on cytokines involved in bone turnover through this signal cascade.
Janus kinase inhibitors role in bone remodeling
TLDR
The role of JAKs inhibitors on bone remodeling and on RANKL‐RANK‐OPG signal and inflammatory cytokines which are involved in the regulation of bone cells, such as osteoblasts and osteoclasts are focused on.
Systemic Jak1 activation causes extrarenal calcitriol production and skeletal alterations provoking stunted growth
TLDR
A mouse model that resembles a constitutive activating mutation of the Jak1/Stat3 signaling pathway in humans shows altered mineral metabolism, and demonstrates that Jak1 is also involved in bone remodeling early in life, probably both, directly and systemically by regulating mineral homeostasis.
JAK2 Inhibition by Fedratinib Reduces Osteoblast Differentiation and Mineralisation of Human Mesenchymal Stem Cells
TLDR
A JAK2 inhibitor (Fedratinib) is identified as a powerful inhibitor of the osteoblastic differentiation of hMSC-TERT cells, which may be useful as a therapeutic option for treating conditions associated with ectopic bone formation or osteosclerotic metastases.
STAT3 controls osteoclast differentiation and bone homeostasis by regulating NFATc1 transcription
TLDR
The data provide the first evidence that STAT3 is significant in osteoclast differentiation and bone homeostasis in vivo, and it may be identified as a potential pharmacological target for the treatment of bone metabolic diseases through regulation of osteOClast activity.
JAK inhibition increases bone mass in steady-state conditions and ameliorates pathological bone loss by stimulating osteoblast function
TLDR
It was determined that JAK inhibitors induced bone repair by altering gene expression and increasing activity of osteoblasts, supporting use of inhibitors as potential osteoanabolics and support that Jaki is a potent therapeutic tool for increasing osteoblast function and bone formation.
Loss of signal transducer and activator of transcription 3 impaired the osteogenesis of mesenchymal progenitor cells in vivo and in vitro
TLDR
Loss of Stat3 impaired the osteogenesis of mesenchymal progenitors in vivo and in vitro, and played a critical role in bone development and osteogenesis.
STAT3 promotes bone fracture healing by enhancing the FOXP3 expression and the suppressive function of regulatory T cells
TLDR
Stat3 was beneficial to bone fracture healing, possibly by enhancing Treg‐mediated suppression of counteracting inflammations, and suggested that STAT3 could be used as a prognostic marker to identify otherwise undistinguishable patients at risk of developing delayed union or nonunion.
MicroRNA-17 Targets JAK1 and STAT3 to Inhibit Osteoblast Differentiation
TLDR
It appears that miR-17 is exhibiting an inhibitory effect on osteogenesis in pre-osteoblast cells by down-regulating JAK1 and STAT3 protein levels.
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