ArticleFrontiers in physiology2012
Mechanistic modeling of aberrant energy metabolism in human disease.
Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Transcriptional Analysis of Nuclear-Encoded Mitochondrial Genes in Eight Neurodegenerative Disorders: The Analysis of Seven Diseases in Reference to Friedreich's Ataxia.Frontiers in genetics · 2021Article
- In vitro Metabolomic Approaches to Investigating the Potential Biological Effects of Phenolic Compounds: An Update.Genomics, proteomics & bioinformatics · 2017Review
- Modelling the molecular mechanisms of aging.Bioscience reports · 2017Review
- HEPNet: A Knowledge Base Model of Human Energy Pool Network for Predicting the Energy Availability Status of an Individual.PloS one · 2015Article
- A conceptual review on systems biology in health and diseases: from biological networks to modern therapeutics.Systems and synthetic biology · 2014Article
- Genome-scale modeling and human disease: an overview.Frontiers in physiology · 2014Article
- The impact of mitochondrial DNA and nuclear genes related to mitochondrial functioning on the risk of Parkinson's disease.Current genomics · 2013Article
- Computational approaches for understanding energy metabolism.Wiley interdisciplinary reviews. Systems biology and medicineReview
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 molecular 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, we review a variety of mechanistic modeling studies that explore metabolic functions, deficiency disorders, and aberrant biochemical pathways in mitochondria and related regions in the cell.
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Registered trials
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