TY - JOUR
T1 - Mechanistic modeling of aberrant energy metabolism in human disease
AU - Sangar, Vineet
AU - Eddy, James A.
AU - Simeonidis, Evangelos
AU - Price, Nathan D.
PY - 2012
Y1 - 2012
N2 - Dysfunction in energy metabolism-including in pathways localized to the mitochondria-has been implicated in the pathogenesis of a wide array of disorders, ranging from cancer to neurodegenerative diseases to type II diabetes. The inherent complexities of energy and mitochondrial metabolism present a significant obstacle in the effort to understand the role that these moleular processes play in the development of disease. To help unravel these complexities, systems biology methods have been applied to develop an array of computational metabolic models, ranging from mitochondria-specific processes to genome-scale cellular networks. These constraint-based (CB) models can efficiently simulate aspects of normal and aberrant metabolism in various genetic and environmental conditions. Development of these models leverages-and also provides a powerful means to integrate and interpret-information from a wide range of sources including genomics, proteomics, metabolomics, and enzyme kinetics. Here, wereview a variety of mechanistic modeling studies that explore metabolic functions, deficiency disorders, and aberrant biochemical pathways in mitochondria and related regionsin the cell.
AB - Dysfunction in energy metabolism-including in pathways localized to the mitochondria-has been implicated in the pathogenesis of a wide array of disorders, ranging from cancer to neurodegenerative diseases to type II diabetes. The inherent complexities of energy and mitochondrial metabolism present a significant obstacle in the effort to understand the role that these moleular processes play in the development of disease. To help unravel these complexities, systems biology methods have been applied to develop an array of computational metabolic models, ranging from mitochondria-specific processes to genome-scale cellular networks. These constraint-based (CB) models can efficiently simulate aspects of normal and aberrant metabolism in various genetic and environmental conditions. Development of these models leverages-and also provides a powerful means to integrate and interpret-information from a wide range of sources including genomics, proteomics, metabolomics, and enzyme kinetics. Here, wereview a variety of mechanistic modeling studies that explore metabolic functions, deficiency disorders, and aberrant biochemical pathways in mitochondria and related regionsin the cell.
KW - Constraint-basedmodels
KW - Energymetabolism
KW - Fluxbalanceanalysis
KW - Mitochondria
KW - Systemsbiology
KW - Warburgeffect
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U2 - 10.3389/fphys.2012.00404
DO - 10.3389/fphys.2012.00404
M3 - Review article
C2 - 23112774
AN - SCOPUS:84870937593
SN - 1664-042X
VL - 3 OCT
JO - Frontiers in Physiology
JF - Frontiers in Physiology
M1 - Article 404
ER -