Sentence examples for mitochondrial dysfunction than from inspiring English sources

Owing to their high-energy metabolic rate, neurons are highly dependent on mitochondria, and therefore, neurons are more vulnerable to mitochondrial dysfunction than other cell types.

Since hepatic dysfunction is a hallmark of sepsis, we hypothesized that the liver is more susceptible to mitochondrial dysfunction than the peripheral tissues, such as the skeletal muscle.

Nevertheless, we think that it is premature to conclude that SAMP strains are degenerative disease models rather than accelerated-senescence models because in vitro studies have shown that primary-cultured cells from several SAMP strains show accelerated senescence and higher oxidative stress and mitochondrial dysfunction than the SAMR1 strain [ 67- 69].

However, a fission fusion cycle defect does not explain why Mfn2 ablation produces greater mitochondrial dysfunction than Mfn1 ablation (see above), or reveal why Parkin translocation defects in neurons and cardiomyocytes are exclusively evoked by Mfn2 deficiency (Lee et al, 2012; Pham et al, 2012; Chen & Dorn, 2013).

Trushina's metabolomics approach revealed that CP2 restored mitochondrial dysfunction rather than directly affecting Aβ formation.

Furthermore, we observed higher quantified relative expressions of cardiac c-caspase 9 over c-caspase 3. It is possible that more mitochondrial dysfunction apoptosis than ER stress-related apoptosis was involved in cardiac pathogenesis of the R6/2 HD mice.

These results indicated that Cd-induced mitochondrial fission occurred earlier than mitochondrial dysfunction, which only changed over a 6-h period in CdCl2-treated L02 cells.

The mechanism responsible for the depressed modulation of O2 consumption by endogenous NO is likely because of the decreased release of NO from the vascular endothelium rather than mitochondrial dysfunction.

These results support the view that Parkin is activated by severe mitochondrial depolarization, rather than by mitochondrial dysfunction per se (24).

This assay reveals latent mitochondrial dysfunction and was more sensitive than histological and biochemical cytochrome c oxidase (COX) activity measurements, which resulted normal in gastrocnemius and in soleus in both genotypes, also after denervation.

Using N2A cells stably expressing mutant form of Bcl-2, it has been described that Bcl-2 regulates the induction of apoptosis mediated by endoplastic reticulum (ER) stress rather than by mitochondrial dysfunction after PrPSc infection (Hetz et al., 2003).