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Entity

Name
mitochondrial dysfunction
Namespace
HBP
Namespace Version
20181212
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/56d6631d06deeead416b3b5100d3b4b8d88c29c6/export/hbp-names.belns

Appears in Networks 3

In-Edges 3

act(a(HBP:"alpha-4 beta-2 nAChR")) increases path(HBP:"mitochondrial dysfunction") View Subject | View Object

Arora et al. (2013) investigated, in a cellular system, the effect of prolonged Abeta exposure on nAChR function. The rodent neuroblastoma cell line NG108-15 was transfected with alpha4beta2 nAChRs and treated for three days with 100 nM Abeta. The following acute stimulation with Abeta and nicotine led to receptor activation that caused a perturbation of intracellular calcium homeostasis followed by mitochondrial dysfunction and increased oxidative stress (Arora et al., 2013) PubMed:25514383

a(CHEBI:"methylene blue") decreases path(HBP:"mitochondrial dysfunction") View Subject | View Object

In mechanistic studies, it was proposed that methylene blue inhibits the Aβ-ABAD interaction and decreases mitochondrial dysfunction by decreasing the expression of ABAD levels, in addition to decreasing Aβ levels. PubMed:30444369

Out-Edges 7

path(HBP:"mitochondrial dysfunction") increases path(MESH:"Alzheimer Disease") View Subject | View Object

Mitochondria are instrumental in the regulation of energy metabolism, and impairment in mitochondrial function has been implicated in the pathogenesis of AD, leading to the mitochondrial cascade hypothesis of AD [121]. PubMed:29758300

path(HBP:"mitochondrial dysfunction") increases path(MESH:"Alzheimer Disease") View Subject | View Object

Altogether, as with proteinopathy, accumulation of damaged or dysfunctional mitochondria is detrimental to the development of AD pathologies PubMed:29758300

path(HBP:"mitochondrial dysfunction") decreases a(CHEBI:ATP) View Subject | View Object

Dysfunctional mitochondria are critically harmful to cells, as this leads to decreased synthesis of cellular ATP and accumulation of ROS, which further overburden and damage other functional mitochondria. PubMed:29758300

path(HBP:"mitochondrial dysfunction") increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Dysfunctional mitochondria are critically harmful to cells, as this leads to decreased synthesis of cellular ATP and accumulation of ROS, which further overburden and damage other functional mitochondria. PubMed:29758300

path(HBP:"mitochondrial dysfunction") increases a(CHEBI:"amyloid-beta") View Subject | View Object

Previous studies demonstrate impaired mitochondrial function preceding the accumulation of hallmark proteins in AD, such as Aβ [123,124] and tau [125]. PubMed:29758300

path(HBP:"mitochondrial dysfunction") increases p(HGNC:MAPT) View Subject | View Object

Previous studies demonstrate impaired mitochondrial function preceding the accumulation of hallmark proteins in AD, such as Aβ [123,124] and tau [125]. PubMed:29758300

path(HBP:"mitochondrial dysfunction") increases bp(GO:mitophagy) View Subject | View Object

Thus, as a quality control mechanism, mitophagy − a form of selective macroautophagy that specifically targets mitochondria − occurs in response to damaged or dysfunctional mitochondria in order to prevent mitochondrial bioenergetic deficits. PubMed:29758300

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.