The ATP deficit is a potential link between mitochondrial abnormality and proteasome deficit, although proteasome deficit could also be caused by other mechanisms such as abnormal post-translational modification including phosphorylation, assembly and targeting, etc. α-synuclein is known to be a target of proteasome degradation in the cytosol [53], [54].
Neuronal loss, cognitive decline, hypometabolism, mitochondrial abnormality, and accumulation of hyperphosphorylated (p-Tau) have been reported in AD brain.
Oncocytic endothelial cells and the related features of subendothelial swelling, basal membrane exposure, mitochondrial abnormality, and phagocytosis were quantified and normalized per image and leukocyte.
We found that loss of SigR1 leads to abnormal ER morphology, mitochondrial abnormalities and impaired autophagic degradation.
Interestingly, allelic loss of the autophagic gene Becn1 delays tumorigenesis in Atm-null mice presumably by reversing the mitochondrial abnormalities and not by improving the DNA damage response (DDR) pathway.
She could not have imagined the technique of mitochondrial replacement - removing the nucleus from an egg with mitochondrial abnormalities, and placing it in a donor egg.
The reduction of the mitochondrial respiratory chain transfer efficiency, electronic leak, and ATP synthesis decline often occurred in aging, leading to mitochondrial abnormalities and alteration of reactive oxygen species levels (Green et al., 2011; Vendelbo and Nair, 2011).
Its primary cause is still controversial, but autoimmune and degenerative processes are assumed to be pathogenically relevant, involving a complex interaction between, for example, environmental triggers, genetic susceptibility, aging, oxidative and endoplasmic reticulum stress, mitochondrial abnormalities and aberrant myoproteostasis [11, 12, 13].
The role of mitochondrial abnormalities and oxidative stress in the etiology of sarcopenia has been extensively characterized [20] [27].
It is also known that progressive mitochondrial abnormalities and apoptotic cell death occur in the hearts of R120G TG mice.
These include the atypical proinsulin disposal and processing, ER and oxidative stress, mitochondrial abnormalities, and β-cell depletion [16], [17] (unpublished observations).
