Wu2007_MitochondrialTCAcycle

This a model from the article:
Computer modeling of mitochondrial tricarboxylic acid cycle, oxidative
phosphorylation, metabolite transport, and electrophysiology.

Wu F, Yang F, Vinnakota KC, Beard DA. J Biol Chem
2007 Aug 24;282(34):24525-37 17591785
,
Abstract:

A computational model of mitochondrial metabolism and electrophysiology is
introduced and applied to analysis of data from isolated cardiac mitochondria
and data on phosphate metabolites in striated muscle in vivo. This model is
constructed based on detailed kinetics and thermodynamically balanced reaction
mechanisms and a strict accounting of rapidly equilibrating biochemical species.
Since building such a model requires introducing a large number of adjustable
kinetic parameters, a correspondingly large amount of independent data from
isolated mitochondria respiring on different substrates and subject to a variety
of protocols is used to parameterize the model and ensure that it is challenged
by a wide range of data corresponding to diverse conditions. The developed model
is further validated by both in vitro data on isolated cardiac mitochondria and
in vivo experimental measurements on human skeletal muscle. The validated model
is used to predict the roles of NAD and ADP in regulating the tricarboxylic acid
cycle dehydrogenase fluxes, demonstrating that NAD is the more important
regulator. Further model predictions reveal that a decrease of cytosolic pH
value results in decreases in mitochondrial membrane potential and a
corresponding drop in the ability of the mitochondria to synthesize ATP at the
hydrolysis potential required for cellular function.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wu F, Yang F, Vinnakota KC, Beard DA. (2007) - version=1.0

The original CellML model was created by:
Geoffrey Nunns

[e-mail]
The University of Auckland
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