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BIOMD0000000278
parameter: metaid_0000037
name: Lemaire2004_BoneRemodeling_RANKRANKLOPGpathway
parameter: metaid_0000028
creator:
  ORG:
    orgname: Scientific Computing and Mathematical Modeling, GlaxoSmithKline, King of Prussia, PA, USA.
  n:
    given: Vincent
    family: Lemaire
parameter: metaid_0000030
parameter: metaid_0000013
parameter: metaid_0000021
volume units: 773761
rule: metaid_0000047
species: metaid_0000006
parameter: metaid_0000033
rule: metaid_0000043
type: SBMLModel
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notes: This a model from the article: Modeling the interactions between osteoblast and osteoclast activities in bone remodeling. Lemaire V, Tobin FL, Greller LD, Cho CR, Suva LJ. J Theor Biol. 2004 Aug 7;229(3):293-309. 15234198 , Abstract: We propose a mathematical model explaining the interactions between osteoblasts and osteoclasts, two cell types specialized in the maintenance of the bone integrity. Bone is a dynamic, living tissue whose structure and shape continuously evolves during life. It has the ability to change architecture by removal of old bone and replacement with newly formed bone in a localized process called remodeling. The model described here is based on the idea that the relative proportions of immature and mature osteoblasts control the degree of osteoclastic activity. In addition, osteoclasts control osteoblasts differentially depending on their stage of differentiation. Despite the tremendous complexity of the bone regulatory system and its fragmentary understanding, we obtain surprisingly good correlations between the model simulations and the experimental observations extracted from the literature. The model results corroborate all behaviors of the bone remodeling system that we have simulated, including the tight coupling between osteoblasts and osteoclasts, the catabolic effect induced by continuous administration of PTH, the catabolic action of RANKL, as well as its reversal by soluble antagonist OPG. The model is also able to simulate metabolic bone diseases such as estrogen deficiency, vitamin D deficiency, senescence and glucocorticoid excess. Conversely, possible routes for therapeutic interventions are tested and evaluated. Our model confirms that anti-resorptive therapies are unable to partially restore bone loss, whereas bone formation therapies yield better results. The model enables us to determine and evaluate potential therapies based on their efficacy. In particular, the model predicts that combinations of anti-resorptive and anabol…
parameter: metaid_0000035
rule: metaid_0000042
created:
  W3 CDTF: Thu Nov 18 11:20:34 GMT 2010
parameter: metaid_0000014
parameter: metaid_0000022
parameter: metaid_0000034
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species: metaid_0000005
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parameter: metaid_0000017
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is: MODEL1006230067
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compartment: metaid_0000003
is version of: GO:0046849
parameter: metaid_0000010
parameter: metaid_0000024
is described by: http://identifiers.org/pubmed/15234198
creator:
  ORG:
    orgname: Scientific Computing and Mathematical Modeling, GlaxoSmithKline, King of Prussia, PA, USA.
  n:
    given: Frank L
    family: Tobin
time units: metaid_0000004
parameter: metaid_0000036
rule: metaid_0000040
rule: metaid_0000041
parameter: metaid_0000027
rule: metaid_0000038
modified:
  W3 CDTF: Fri Apr 20 23:12:04 BST 2012
substance units: metaid_0000060
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creator:
  ORG:
    orgname: EMBL-EBI
  n:
    given: Vijayalakshmi
    family: Chelliah
parameter: metaid_0000020
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rule: metaid_0000045
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area units: metaid_0000005
occurs in: http://identifiers.org/taxonomy/7711
parameter: metaid_0000015
length unit: 879216
parameter: metaid_0000025
parameter: metaid_0000019

metaid_0000013
constant: false
value: NaN
name: Phi_L
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metaid_0000024
is: SBO:0000188
constant: true
value: 200000.0
name: K_O_P
type: Parameter