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Moreover, there is strong evidence that both mitochondrial dysfunction and oxidative stress are causal factors in the pathophysiology of these disorders [37], [38], [39].
There is increasing evidence showing that both mitochondrial dysfunction and oxidative damage play a key role in the pathogenesis of neurodegenerative diseases such as Parkinson's disease (PD) and Huntington's disease (HD) [1], [2].
Oxidative stress results from insufficient scavenging of reactive oxygen species and is reported to be the cause of the selective degeneration of DArgic neurons in PD through both mitochondrial dysfunction and apoptosis [4].
20 Ox-LDL-related peroxyl radical formation is implicated in both mitochondrial dysfunction and macrophage lysis.
Importantly, our data also suggest that both mitochondrial dysfunction and changes in mitochondrial morphology are early, specific consequences of PINK1 deficiency that do not progress further with age.
Down-regulation of hnRNP A1 was found to suppress both mitochondrial dysfunction and cell death in 3-NP-treated cells, while, the over-expression of hnRNP A1 enhanced Drp1 expression and increased mitochondrial fragmentation.
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Median interstitial fluid glucose was lower in ischemia (2 mmol/l) compared with both mitochondrial dysfunction (4 mmol/l) and with no ischemia/mitochondrial dysfunction (5 mmol/l) (P < 0.001).
The toxicity impact of both drugs extensively involved mitochondrial dysfunction and damage, and also fatty acid metabolism and PPARα/RXRα activation.
MAO inhibition by pargyline significantly reduced both ROS accumulation and mitochondrial dysfunction, and normalized the increased incidence of apoptosis in myoblasts from patients.
Expression of mutant HTT and 3-NP treatment trigger both mitochondrial fission and mitochondrial dysfunction, and eventually induce neurotoxicity with disrupted axonal transport and synaptic degeneration [10], [11], [12], [13], [14], [15].
However, the degree of nuclear genomic instability can be linked to mitochondrial dysfunction and both defects together can contribute to tumor progression.
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both thyroid dysfunction and
both microcirculatory dysfunction and
both political dysfunction and
both mitochondrial fission and
both renal dysfunction and
both mitochondrial density and
both placental dysfunction and
both ventricular dysfunction and
both cognitive dysfunction and
both autonomic dysfunction and
both lysosome dysfunction and
both mitochondrial dysregulation and
both telomere dysfunction and
both mitochondrial inheritance and
both contractile dysfunction and
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