Mitochondrial Dysfunction in Neural Injury

Zhao, Xiu-Yun; Lu, Mei-Hong; Yuan, De-Juan; Xu, De-En; Yao, Pei-Pei; Wyatt, J I; Chen, Hong; Liu, Wenlong; Yan, Chen-Xiao; Xia, Yiyuan; Li, Shao; Tao, Jin; Ma, Quanhong

doi:10.3389/fnins.2019.00030

Cited by 97 publications

(66 citation statements)

References 190 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Dysfunction of Respiratory Complex I can cause a number of diseases including MELAS syndrome, Parkinsonism, Leber's disease, and Leigh syndrome (Rodenburg, 2016). In addition to mutant load, cells at particular risk of mitochondrial dysfunction are those that have high energy requirements such as the cerebrum, muscles, and neurons (Zhao et al, 2019). Therefore, in some tissues where energy requirements are lower, the cells are not diseased, whereas in others with high ATP demand, the mutant load may be high enough to cause disease e.g.…”

Section: Mitochondrial Disease Modelling In Dictyostelium Mitochondrimentioning

confidence: 99%

The Dictyostelium model for mitochondrial biology and disease

Pearce¹,

Annesley²,

Fisher³

2019

Int. J. Dev. Biol.

View full text Add to dashboard Cite

The unicellular slime mould Dictyostelium discoideum is a valuable eukaryotic model organism in the study of mitochondrial biology and disease. As a member of the Amoebozoa, a sister clade to the animals and fungi, Dictyostelium mitochondrial biology shares commonalities with these organisms, but also exhibits some features of plants. As such it has made significant contributions to the study of eukaryotic mitochondrial biology. This review provides an overview of the advances in mitochondrial biology made by the study of Dictyostelium and examines several examples where Dictyostelium has and will contribute to the understanding of mitochondrial disease. The study of Dictyostelium's mitochondrial biology has contributed to the understanding of mitochondrial genetics, transcription, protein import, respiration, morphology and trafficking, and the role of mitochondria in cellular differentiation. Dictyostelium is also proving to be a versatile model organism in the study both of classical mitochondrial disease e.g. Leigh syndrome, and in mitochondria-associated neurodegenerative diseases like Parkinson's disease. The study of mitochondrial diseases presents a unique challenge due to the cryptic nature of their genotypephenotype relationship. The use of Dictyostelium can contribute to resolving this problem by providing a genetically tractable, haploid eukaryotic organism with a suite of readily characterised phenotype readouts of cellular signalling pathways. Dictyostelium has provided insight into the signalling pathways involved in multiple neurodegenerative diseases and will continue to provide a significant contribution to the understanding of mitochondrial biology and disease.

show abstract

Section: Mitochondrial Disease Modelling In Dictyostelium Mitochondrimentioning

confidence: 99%

The Dictyostelium model for mitochondrial biology and disease

Pearce¹,

Annesley²,

Fisher³

2019

Int. J. Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…Mitochondria of brain and neurons are affected by HPX, because ATP generation bioenergetic requires oxygen consumption in mitochondria (Thornton et al 2017). Mitochondria is a main source of reactive oxygen species (ROS) generation (Zhao et al 2019). Accumulating evidence indicates that the hypoxia and ischemic conditions result in excessive ROS generation, inflammation and apoptosis through the increase of membrane depolarization in mitochondria of neurons (Sun et al 2014;Yang et al 2019 (Caterina et al 1997).…”

Section: Introductionmentioning

confidence: 99%

Levetiracetam modulates hypoxia-induced inflammation and oxidative stress via inhibition of TRPV1 channel in the DBTRG glioblastoma cell line

Ertilav

2020

Journal of Cellular Neuroscience and Oxidative Stress

View full text Add to dashboard Cite

show abstract

“…Insulin signaling mediates glucose metabolism and mitochondrial physiology (Cheng et al, 2010). Additionally, mitochondrial alterations are related with synapse dysfunction and neurodegeneration (Zhao et al, 2019) . Therefore, we investigated if GB progression affects neuronal mitochondria.…”

Section: Gbmentioning

confidence: 99%

Insulin signaling mediates neurodegeneration in glioma

Jarabo

Pablo

Herranz

et al. 2020

Preprint

View full text Add to dashboard Cite

Cell to cell communication facilitates tissue development and physiology. Under pathological conditions, brain tumors disrupt glia-neuron communication signals in which in consequence, promotes tumor expansion at expenses of healthy tissue. The glioblastoma is the most aggressive and frequent brain tumor. This type of glioma expands and infiltrates in the brain, causing neuronal degeneration and neurological decay, among other symptoms. Here we describe how glioblastoma produce ImpL2, an antagonist of the insulin pathway, which is regulated by the microRNA miR-8. ImpL2 targets neighboring neurons and causes mitochondrial disruption as well as synapse loss, an early symptom of neurodegeneration. Furthermore, glioblastoma progression requires insulin pathway attenuation in neurons. Restoration of neuronal insulin activity is sufficient to rescue this synapse loss and delay the premature death caused by glioma. Therefore, signals from GB to neuron emerge as a potential field of study to prevent neurodegeneration and anti-tumoral strategies. A. (2006). Age-independent synaptogenesis by phosphoinositide 3 kinase.

show abstract

Mitochondrial Dysfunction in Neural Injury

Cited by 97 publications

References 190 publications

The Dictyostelium model for mitochondrial biology and disease

The Dictyostelium model for mitochondrial biology and disease

Levetiracetam modulates hypoxia-induced inflammation and oxidative stress via inhibition of TRPV1 channel in the DBTRG glioblastoma cell line

Insulin signaling mediates neurodegeneration in glioma

Contact Info

Product

Resources

About