vanBeek2007_OxPhos_HeartMuscleCells

This a model from the article:
Adenine nucleotide-creatine-phosphate module in myocardial metabolic system
explains fast phase of dynamic regulation of oxidative phosphorylation.

van Beek JH. Am J Physiol Cell Physiol
2007 Sep;293(3):C815-29 17581855
,
Abstract:

Computational models of a large metabolic system can be assembled from modules
that represent a biological function emerging from interaction of a small subset
of molecules. A "skeleton model" is tested here for a module that regulates the
first phase of dynamic adaptation of oxidative phosphorylation (OxPhos) to
demand in heart muscle cells. The model contains only diffusion, mitochondrial
outer membrane (MOM) permeation, and two isoforms of creatine kinase (CK), in
cytosol and mitochondrial intermembrane space (IMS), respectively. The
communication with two neighboring modules occurs via stimulation of
mitochondrial ATP production by ADP and P(i) from the IMS and via time-varying
cytosolic ATP hydrolysis during contraction. Assuming normal cytosolic diffusion
and high MOM permeability for ADP, the response time of OxPhos (t(mito);
generalized time constant) to steps in cardiac pacing rate is predicted to be
2.4 s. In contrast, with low MOM permeability, t(mito) is predicted to be 15 s.
An optimized MOM permeability of 21 mum/s gives t(mito) = 3.7 s, in agreement
with experiments on rabbit heart with blocked glycolytic ATP synthesis. The
model correctly predicts a lower t(mito) if CK activity is reduced by 98%. Among
others, the following predictions result from the model analysis: 1) CK activity
buffers large ADP oscillations; 2) ATP production is pulsatile in beating heart,
although it adapts slowly to demand with "time constant" approximately 14
heartbeats; 3) if the muscle isoform of CK is overexpressed, OxPhos reacts
slower to changing workload; and 4) if mitochondrial CK is overexpressed, OxPhos
reacts faster.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
van Beek JH. (2007) - version=1.0

The original CellML model was created by:
Catherine Lloyd

[e-mail]
The University of Auckland
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