Mitochondrial control of cell bioenergetics in Parkinson's disease.
Parkinson disease (PD) is a neurodegenerative disorder characterized by a selective loss of dopaminergic neurons in the substantia nigra. The earliest biochemical signs of the disease involve failure in mitochondrial-endoplasmic reticulum cross talk and lysosomal function, mitochondrial electron chain impairment, mitochondrial dynamics alterations, and calcium and iron homeostasis abnormalities. These changes are associated with increased mitochondrial reactive oxygen species (mROS) and energy deficiency. Recently, it has been reported that, as an attempt to compensate for the mitochondrial dysfunction, neurons invoke glycolysis as a low-efficient mode of energy production in models of PD. Here, we review how mitochondria orchestrate the maintenance of cellular energetic status in PD, with special focus on the switch from oxidative phosphorylation to glycolysis, as well as the implication of endoplasmic reticulum and lysosomes in the control of bioenergetics.
Department of Biochemistry and Molecular Biology, University of Cordoba, Institute Maimonides of Biomedical Investigation of Cordoba (IMIBIC), Cordoba, Spain.
Raquel
R
Requejo-Aguilar
Institute of Functional Biology and Genomics (IBFG), University of Salamanca-CSIC, Zacarias Gonzalez, 2, 37007 Salamanca, Spain. Electronic address: jbolanos@usal.es.
Juan P
JP
Bolaños
D000818:Animals; D059290:Dopaminergic Neurons / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism; D004734:Energy Metabolism; D006801:Humans; D008247:Lysosomes / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D010300:Parkinson Disease / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013378:Substantia Nigra / Q000378:metabolism
D017382:Reactive Oxygen Species
Autophagy; Glycolysis; Lysosome; Mitochondria; Neurodegeneration; Parkinson’s disease; Pentose-phosphate pathway; Redox