Showing papers in "Mitochondrion in 2012"

TL;DR: In this paper, it was shown that endoplasmic reticulum and peroxisomes have a greater capacity to produce ROS than mitochondria, at least in liver.

TL;DR: Decreased miR-181a levels reduced glucose deprivation induced apoptosis, mitochondrial dysfunction, and loss of mitochondrial membrane potential in astrocytes.

TL;DR: Molecular VDAC appears to be a convergence point for a variety of cell survival and cell death signals, mediated by its association with various ligands and proteins, and insight is provided into the potential of VDac1 as a rational target for novel therapeutics.

TL;DR: Light is shed on the molecular identity of the main proteins involved in the handling of mitochondrial Ca2+ traffic, opening fascinating and ambitious new avenues for mitochondria-based pharmacological strategies.

TL;DR: Mitochondrial dysfunction has been identified as one potential cause of epileptic seizures and mitochondria have to be considered as promising targets for neuroprotective strategies in epilepsy.

TL;DR: It is demonstrated that Pi activates MPTP opening under all energised and de-energised conditions tested while CsA inhibits pore opening whether or not Pi is present.

TL;DR: The current literature on retrograde signalling in both yeast and mammalian cells is reviewed, with an outlook on its potential contribution to disease through the regulation of PGC-1 family coactivators.

TL;DR: This review describes this concept and summarizes different approaches used to regulate mitochondrial respiration by targeting complex I as a proximal site in the electron transport chain (ETC) in order to favor the cytoprotection.

TL;DR: Cytochrome c oxidase (COX) represents the rate-limiting enzyme of the mitochondrial respiratory chain and is thus predestined for being a central site of regulation of oxidative phosphorylation, proton pumping efficiency, ATP and reactive oxygen species production, which in turn affect cell signaling and survival.

TL;DR: This review is focussed on the recent studies demonstrating the presence of miRNAs in mitochondria and its possible significance in different cellular and physiological conditions.

TL;DR: Results demonstrate that first level screening based on microscale oxygraphy is more sensitive, cheaper and rapid than spectrophotometry for the biochemical evaluation of cells from patients with suspected mitochondrial disorders.

TL;DR: It is proposed that a variety of genes may each confer a background susceptibility to POAG in different populations having one common link: mitochondrial dysfunction, which contributes to the pathogenesis of POAG.

TL;DR: A variety of functionalized nanosystems including polymeric and metallic nanoparticles as well as liposomes are more effective than plain drug and non-functionalized nanOSystems in delivering therapeutic agents to mitochondria.

TL;DR: The results show that mitochondria are an important ROS source in skeletal muscle cells and the substantial changes in mitochondrial ROS synthesis during skeletal muscle differentiation can be explained by intensive bioenergetic remodeling.

TL;DR: A custom-made STimulated Emission Depletion (STED) fluorescence nanoscope with ~30nm lateral resolution is used for protein mapping of Percoll-purified viable mitochondria from murine heart and is able to quantify and resolve distinct protein clusters within mitochondria.

TL;DR: A failure in tRNA metabolism caused by these tRNA mutations impaired mitochondrial translation and respiration, thereby causing mitochondrial dysfunctions responsible for deafness, offer valuable information for the early diagnosis, management and treatment of maternally inherited deafness.

TL;DR: It is proposed that an interplay between defective mitochondrial morphology and clearance arises as a crucial player in sentencing neuronal fate in Parkinson's disease.

TL;DR: The effects of neonatal hypoxia-ischemia on energy metabolism in male and female rats were investigated, suggesting a dimorphism in mitochondrial dysfunction and information that may lead to new neuroprotection strategies.

TL;DR: The results show that a small set of naturally occurring mtDNA mutations can have a significant influence on mitochondrial bioenergetics that may change as the organism ages.

TL;DR: In this paper, the changes in mitochondrial presence within axons in relation to the presence or absence of healthy myelin sheaths are discussed and the increase in mitochondria presence following demyelination is proposed as an adaptive process.

TL;DR: It is demonstrated that PEI in a concentration- and time-dependent manner can affect functions (membrane potential, swelling and respiration) and ultrastructural integrity of freshly isolated rat liver mitochondria and shows an uncoupling property that is detectable at low respiration rates.

TL;DR: The structural damage grading here described could provide new insight on IDC mitochondrial impairment and represent hallmark in the breast cancer mitochondriopathy.

TL;DR: SirT1 protein is described as a metabolic protein that can sense and communicate the energy status of a cell to key mechanisms of mitochondrial regulation and energy production that allow for the design of pharmaceuticals for the treatment of degenerative processes that are associated with metabolic and mitochondrial health.

TL;DR: It is shown that homozygous and heterozygous Cox7a1 knockout mice, although viable, have reduced Cox activity and develop a dilated cardiomyopathy at 6 weeks of age, and, surprisingly, the cardiopathy improves and stabilizes by 6 months of age.

TL;DR: The functional involvement of sirtuins as sensors of the redox/nutritional state of mitochondria and their role in mitochondrial protection against stress are described, suggesting that pharmacological manipulation of sIRTuins is a viable strategy against several pathologies.

TL;DR: mRNAs encoding hydrophobic OXPHOS proteins, which insert into the inner membrane, were localized near mitochondria and gene which mRNAs were predominantly localized in cytosol had less than one transmembrane domain.

TL;DR: The current knowledge concerning the consequences of nDNA-encoded CI mutations in patient-derived cells, present mouse models for human CI deficiency, and discuss potential treatment strategies for CI deficiency are summarized.

TL;DR: Using lectin chromatography on bovine heart, low-abundance glycoforms of nuclear-encoded proteins with well-established mitochondrial function are detected, indicating that glycosylation of classic mitochondrial proteins may be more common than previously appreciated.

TL;DR: These studies provide a biochemical basis for nNOS mediated oligodendrocyte injury and suggest similar mechanisms may play a role in diseases characterized by oligodendedrocytes loss and demyelination.

TL;DR: Flow cytometry analysis studied reactive oxygen species (ROS) production of yeast frataxin mutant cells treated with two antioxidants, N-acetyl-L-cysteine and a mitochondrially-targeted analog of vitamin E, confirming that mitochondria are the main site of ROS production in this model.