Disruption of the subtle balance between protein synthesis and degradation during muscle atrophy involves the suppression of bioenergetic pathways associated to mitochondrial functions and controlled by PGC-1α whose expression is sharply reduced in various models of muscle wasting [ 17– 17].
The Gu Lab investigates the evolution of mitochondrial functions and the role of mtDNA mutation in aging and various diseases, including but not limited to tumor, autism and neural degenerative diseases.
In this study, we investigate the role of HIF activation on lidocaine-induced apoptosis in renal cell-derived RCC4 cells lacking functional VHL and neuronal SH-SY5Y cells exposed to nPG, DFX, or hypoxia and describe that activation of HIF-1 alleviates lidocaine toxicity by suppressing mitochondrial functions and generating ROS.
Mitochondrial functions and architecture rely on a defined lipid composition of their outer and inner membranes, which are characterized by a high content of non-bilayer phospholipids such as cardiolipin (CL) and phosphatidylethanolamine (PE).
TiO2 NPs impair mitochondrial functions and lead to OS in the rat and mouse brain [64, 65].
The effects of trichothecenes on eukaryotic cells include the inhibition of protein, DNA and RNA synthesis, inhibition of mitochondrial functions and cell division, and membrane effects [14, 16].
Huang et al. overexpressed PPARγ coactivator 1α (PGC-1α), which is the master regulator of mitochondrial biogenesis, in MSCs and observed a significant increase in genes related to mitochondrial functions and lipid metabolism (Huang et al., 2011).
nuclear factor kappa B. The authors thank Dr. Hiroyuki Uchida for providing information on the method and for measuring NOx levels, Mr. Kousuke Kazama for providing information on the method and measuring of NAG levels, Ms. Miwa Sugawara for providing information on the method and measuring of muscle mitochondrial functions, and Ms. Chikako Murata for technical assistance.
The latter promote apoptosis by altering mitochondrial functions and activating the release of downstream apoptogenic factors [19].
However, the exact mechanisms of cyclin B1/Cdk1-mediated mitochondrial functions and their potential correlations with p53 are still unknown.
This blocking effect, in turn, led to preservation of mitochondrial functions, and eventually suppression of caspase activity and apoptosis.
