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Mitochondrial dysfunction

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https://www.readbyqxmd.com/read/28102843/il-17-mediated-mitochondrial-dysfunction-impairs-apoptosis-in-rheumatoid-arthritis-synovial-fibroblasts-through-activation-of-autophagy
#1
Eun Kyung Kim, Jeong-Eun Kwon, Seon-Young Lee, Eun-Jung Lee, Da Som Kim, Su-Jin Moon, Jennifer Lee, Seung-Ki Kwok, Sung-Hwan Park, Mi-La Cho
Fibroblast-like synoviocytes (FLSs) are a major cell population of the pannus that invades cartilage and bone in rheumatoid arthritis (RA). FLS resistance to apoptosis is a major characteristic of RA. The aims of this study were to investigate the effects of interleukin-17 (IL-17) and IL-17-producing T helper (Th17) cells on resistance to apoptosis in FLSs from RA patients (RA FLSs) and their roles in mitochondrial dysfunction and autophagy. Mitochondrial function was assessed in RA FLSs and FLSs from osteoarthritis patients (OA FLSs)...
January 19, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28102525/environmental-chemicals-and-aging
#2
REVIEW
Brandon L Pearson, Dan Ehninger
PURPOSE OF REVIEW: Innovations in agriculture and medicine as well as industrial and domestic technologies are essential for the growing and aging global population. These advances generally require the use of novel natural or synthetic chemical agents with the potential to affect human health. Here, we attempt to highlight environmental chemicals and select drugs with the potential to exacerbate aging by directly affecting molecular aging cascades focusing particular attention on the brain...
January 19, 2017: Current Environmental Health Reports
https://www.readbyqxmd.com/read/28101459/venlafaxine-induced-cytotoxicity-towards-isolated-rat-hepatocytes-involves-oxidative-stress-and-mitochondrial-lysosomal-dysfunction
#3
Elham Ahmadian, Hossein Babaei, Alireza Mohajjel Nayebi, Aziz Eftekhari, Mohammad Ali Eghbal
Purpose: Depression is a public disorder worldwide. Despite the widespread use of venlafaxine in the treatment of depression, it has been associated with the incidence of toxicities. Hence, the goal of the current investigation was to evaluate the mechanisms of venlafaxine-induced cell death in the model of the freshly isolated rat hepatocytes. Methods: Collagenase-perfused rat hepatocytes were treated with venlafaxine and other agents. Cell damage, reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial membrane potential decline, lysosomal damage, glutathione (GSH) level were analyzed...
December 2016: Advanced Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/28100843/pathophysiology-and-molecular-basis-of-selected-metabolic-abnormalities-in-huntington-s-disease
#4
Jolanta Krzysztoń-Russjan
Huntington's disease (HD) is an incurable, devastating neurodegenerative disease with a known genetic background and autosomally dominant inheritance pattern. HTT gene mutation (mHTT) is associated with polymorphic fragment elongation above 35 repeats of the CAG triplet. The mHTT product is an altered protein with a poly-Q elongated fragment, with the highest expression determined in the central nervous system (CNS) and with differentiated expression outside the CNS. A drastic loss of striatal and deeper layers of the cerebral cortex neurons was determined in the CNS, but muscle and body weight mass loss with dysfunction of many organs was also observed...
December 30, 2016: Postȩpy Higieny i Medycyny Doświadczalnej
https://www.readbyqxmd.com/read/28100774/loss-of-cyclin-dependent-kinase-2-in-the-pancreas-links-primary-%C3%AE-cell-dysfunction-to-progressive-depletion-of-%C3%AE-cell-mass-and-diabetes
#5
So Yoon Kim, Ji-Hyeon Lee, Matthew J Merrins, Oksana Gavrilova, Xavier Bisteau, Philipp Kaldis, Leslie S Satin, Sushil G Rane
The failure of pancreatic islet β-cells is a major contributor to the etiology of Type 2 diabetes. β-cell dysfunction and declining β-cell mass are two mechanisms that contribute to this failure, although it is unclear if they are molecularly linked. Here, we show that the cell cycle regulator, cyclin-dependent kinase 2 (Cdk2), couples primary β-cell dysfunction to the progressive deterioration of β-cell mass in diabetes. Mice with pancreas-specific deletion of Cdk2 are glucose intolerant primarily due to defects in glucose-stimulated insulin secretion...
January 18, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28100752/differential-vulnerability-of-ca1-versus-ca3-pyramidal-neurons-after-ischemia-possible-relationship-to-sources-of-zn2-accumulation-and-its-entry-into-and-prolonged-effects-on-mitochondria
#6
Yuliya V Medvedeva, Sung G Ji, Hong Z Yin, John H Weiss
: Excitotoxic mechanisms contribute to the degeneration of hippocampal pyramidal neurons after recurrent seizures and brain ischemia. However, susceptibility differs, with CA1 neurons degenerating preferentially after global ischemia and CA3 neurons after limbic seizures. Whereas most studies address contributions of excitotoxic Ca(2+) entry, it is apparent that Zn(2+) also contributes, reflecting accumulation in neurons either after synaptic release and entry through postsynaptic channels or upon mobilization from intracellular Zn(2+)-binding proteins such as metallothionein-III (MT-III)...
January 18, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28098754/drp1-dependent-mitochondrial-fission-plays-critical-roles-in-physiological-and-pathological-progresses-in-mammals
#7
REVIEW
Chenxia Hu, Yong Huang, Lanjuan Li
Current research has demonstrated that mitochondrial morphology, distribution, and function are maintained by the balanced regulation of mitochondrial fission and fusion, and perturbation of the homeostasis between these processes has been related to cell or organ dysfunction and abnormal mitochondrial redistribution. Abnormal mitochondrial fusion induces the fragmentation of mitochondria from a tubular morphology into pieces; in contrast, perturbed mitochondrial fission results in the fusion of adjacent mitochondria...
January 13, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28098577/mitochondria-initiate-and-regulate-sarcopenia
#8
Stephen E Alway, Junaith S Mohamed, Matthew J Myers
We present the hypothesis that an accumulation of dysfunctional mitochondria initiates a signaling cascade leading to motor neuron and muscle fiber death and culminating in sarcopenia. Interactions between neural and muscle cells that contain dysfunctional mitochondria exacerbate sarcopenia. Preventing sarcopenia will require identifying mitochondrial sources of dysfunction that are reversible.
January 16, 2017: Exercise and Sport Sciences Reviews
https://www.readbyqxmd.com/read/28096879/association-between-mitofusin-2-gene-polymorphisms-and-late-onset-alzheimer-s-disease-in-the-korean-population
#9
Young Jong Kim, Jin Kyung Park, Won Sub Kang, Su Kang Kim, Changsu Han, Hae Ri Na, Hae Jeong Park, Jong Woo Kim, Young Youl Kim, Moon Ho Park, Jong-Woo Paik
OBJECTIVE: Mitochondrial dysfunction is a prominent and early feature of Alzheimer's disease (AD). The morphologic changes observed in the AD brain could be caused by a failure of mitochondrial fusion mechanisms. The aim of this study was to investigate whether genetic polymorphisms of two genes involved in mitochondrial fusion mechanisms, optic atrophy 1 (OPA1) and mitofusin 2 (MFN2), were associated with AD in the Korean population by analyzing genotypes and allele frequencies. METHODS: One coding single nucleotide polymorphism (SNP) in the MFN2, rs1042837, and two coding SNPs in the OPA1, rs7624750 and rs9851685, were compared between 165 patients with AD (83 men and 82 women, mean age 72...
January 2017: Psychiatry Investigation
https://www.readbyqxmd.com/read/28096454/mitochondrial-function-is-required-for-extracellular-atp-induced-nlrp3-inflammasome-activation
#10
Daichi Sadatomi, Kazutaka Nakashioya, Sayaka Mamiya, Shino Honda, Yuka Kameyama, Yasuo Yamamura, Susumu Tanimura, Kohsuke Takeda
The NLRP3 inflammasome plays a critical role in the processing and release of inflammatory cytokines, such as interleukin-1β (IL-1β) and IL-18. Accumulating evidence suggests that mitochondria are common mediators of NLRP3 inflammasome activation induced by a wide range of inflammatory stimuli; however, the precise role of mitochondria is still not fully understood. Here, we show that mitochondrial function is required for extracellular ATP-induced NLRP3 inflammasome activation. Extracellular ATP induced the loss of mitochondrial membrane potential and mitochondrial fragmentation in a different manner than other stimuli in primary mouse macrophages...
January 17, 2017: Journal of Biochemistry
https://www.readbyqxmd.com/read/28096230/haemodialysis-in-acute-paracetamol-poisoning
#11
L Serjeant, J Evans, F Sampaziotis, W G Petchey
A woman aged 23 years presented late with clinical and biochemical features of a life-threatening paracetamol (acetaminophen) overdose. Despite instigating N-acetylcysteine treatment, due to evidence of mitochondrial dysfunction together with an exceedingly high paracetamol level, the decision was made to dialyse the patient acutely to remove the parent drug. This was highly effective, and with on-going supportive care, the patient made a full recovery without the need for transplantation. This case highlights the role of extracorporeal therapy as a treatment option in selected cases of paracetamol overdose, consistent with the international guidelines...
January 17, 2017: BMJ Case Reports
https://www.readbyqxmd.com/read/28095860/mouse-models-of-atherosclerosis-a-historical-perspective-and-recent-advances
#12
REVIEW
Yee Ting Lee, Hiu Yu Lin, Yin Wah Fiona Chan, Ka Hou Christien Li, Olivia Tsz Ling To, Bryan P Yan, Tong Liu, Guangping Li, Wing Tak Wong, Wendy Keung, Gary Tse
Atherosclerosis represents a significant cause of morbidity and mortality in both the developed and developing countries. Animal models of atherosclerosis have served as valuable tools for providing insights on its aetiology, pathophysiology and complications. They can be used for invasive interrogation of physiological function and provide a platform for testing the efficacy and safety of different pharmacological therapies. Compared to studies using human subjects, animal models have the advantages of being easier to manage, with controllable diet and environmental risk factors...
January 17, 2017: Lipids in Health and Disease
https://www.readbyqxmd.com/read/28095372/impaired-mitochondrial-respiration-in-large-cerebral-arteries-of-rats-with-type-2-diabetes
#13
Ivan Merdzo, Ibolya Rutkai, Venkata N L R Sure, Catherine A McNulty, Prasad V G Katakam, David W Busija
Mitochondrial dysfunction has been suggested as a potential underlying cause of pathological conditions associated with type 2 diabetes (T2DM). We have previously shown that mitochondrial respiration and mitochondrial protein levels were similar in the large cerebral arteries of insulin-resistant Zucker obese rats and their lean controls. In this study, we extend our investigations into the mitochondrial dynamics of the cerebral vasculature of 14-week-old Zucker diabetic fatty obese (ZDFO) rats with early T2DM...
January 18, 2017: Journal of Vascular Research
https://www.readbyqxmd.com/read/28095320/lethal-dysregulation-of-energy-metabolism-during-embryonic-vitamin-e-deficiency
#14
Melissa McDougall, Jaewoo Choi, Hye-Kyeong Kim, Gerd Bobe, J Frederik Stevens, Enrique Cadenas, Robert Tanguay, Maret G Traber
Vitamin E (α-tocopherol, VitE) was discovered in 1922 for its role in preventing embryonic mortality. We investigated the underlying mechanisms causing lethality using targeted metabolomics analyses of zebrafish VitE-deficient embryos over five days of development, which coincided with their increased morbidity and mortality. VitE deficiency resulted in peroxidation of docosahexaenoic acid (DHA), depleting DHA-containing phospholipids, especially phosphatidylcholine, which also caused choline depletion. This increased lipid peroxidation also increased NADPH oxidation, which depleted glucose by shunting it to the pentose phosphate pathway...
January 14, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28094765/selective-antagonism-of-muscarinic-receptors-is-neuroprotective-in-peripheral-neuropathy
#15
Nigel A Calcutt, Darrell R Smith, Katie Frizzi, Mohammad Golam Sabbir, Subir K Roy Chowdhury, Teresa Mixcoatl-Zecuatl, Ali Saleh, Nabeel Muttalib, Randy Van der Ploeg, Joseline Ochoa, Allison Gopaul, Lori Tessler, Jürgen Wess, Corinne G Jolivalt, Paul Fernyhough
Sensory neurons have the capacity to produce, release, and respond to acetylcholine (ACh), but the functional role of cholinergic systems in adult mammalian peripheral sensory nerves has not been established. Here, we have reported that neurite outgrowth from adult sensory neurons that were maintained under subsaturating neurotrophic factor conditions operates under cholinergic constraint that is mediated by muscarinic receptor-dependent regulation of mitochondrial function via AMPK. Sensory neurons from mice lacking the muscarinic ACh type 1 receptor (M1R) exhibited enhanced neurite outgrowth, confirming the role of M1R in tonic suppression of axonal plasticity...
January 17, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28093764/pre-ischemic-mitochondrial-substrate-constraint-by-inhibition-of-malate-aspartate-shuttle-preserves-mitochondrial-function-after-ischemia-reperfusion
#16
Nichlas Riise Jespersen, Takashi Yokota, Nicolaj Brejnholt Støttrup, Andreas Bergdahl, Kim Bolther Paelestik, Jonas Agerlund Povlsen, Flemming Dela, Hans Erik Bøtker
Mitochondrial dysfunction plays a central role in ischemia-reperfusion (IR) injury. The pre-ischemic administration of aminooxyacetate (AOA), an inhibitor of the malate-aspartate shuttle (MAS), provides cardioprotection against IR injury, but the underlying mechanism remains unknown. We hypothesized that a transient inhibition of the MAS during ischemia and early reperfusion could preserve mitochondrial function at later phase of reperfusion in IR-injured heart to the same extent as ischemic preconditioning (IPC), which is a well-validated cardioprotective strategy against IR injury...
January 17, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28093354/low-dose-resveratrol-ameliorates-mitochondrial-respiratory-dysfunction-and-enhances-cellular-reprogramming
#17
Yuki Mizuguchi, Hideyuki Hatakeyama, Kou Sueoka, Mamoru Tanaka, Yu-Ichi Goto
Mitochondrial disease is associated with a wide variety of clinical presentations, even among patients carrying heteroplasmic mitochondrial DNA (mtDNA) mutations, probably because of variations in mutant mtDNA proportions at the tissue and organ levels. Although several case reports and clinical trials have assessed the effectiveness of various types of drugs and supplements for the treatment of mitochondrial diseases, there are currently no cures for these conditions. In this study, we demonstrated for the first time that low dose resveratrol (RSV) ameliorated mitochondrial respiratory dysfunction in patient-derived fibroblasts carrying homoplasmic mtDNA mutations...
January 13, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28093254/risperidone-ameliorated-a%C3%AE-1-42-induced-cognitive-and-hippocampal-synaptic-impairments-in-mice
#18
Lingzhi Wu, Xiaowen Feng, Tingting Li, Baojuan Sun, Muhammad Zahid Khan, Ling He
Alzheimer's disease (AD) is a complex neurodegenerative disorder with cognitive impairment and major neuropathologic hallmark of amyloid-beta (Aβ) peptides. Risperidone, an atypical antipsychotic, can improve concentration and cognitive deficit in schizophrenia patients. In this study, behavior tests including Morris Water Maze test, Step-through passive avoidance test, Open Field test, Step-Down test, Hole-Board test and Novel object recognition test were preformed to examine the effect of Risperidone on Aβ1-42-induced cognitive dysfunction in both long-term and short-term memory...
January 13, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28093052/erk-nrf2-ho-1-pathway-mediated-mitophagy-alleviates-traumatic-brain-injury-induced-intestinal-mucosa-damage-and-epithelial-barrier-dysfunction
#19
Yinlong Liu, Zhongyuan Bao, Xiupeng Xu, Honglu Chao, Chao Lin, Zheng Li, Yan Liu, Xiaoming Wang, Yongping You, Ning Liu, Jing Ji
Gastrointestinal dysfunction is one of several physiologic complications in patients with traumatic brain injury (TBI). TBI can result in increased intestinal permeability due to apoptosis of intestinal epithelial cells, which contain a large number of mitochondria for persisting barrier function. Autophagy of damaged mitochondria (mitophagy) controls the quality of the mitochondria and regulates cellular homeostasis. However, the exact mechanism of mitophagy that underlies the pathological changes induced by TBI is unknown...
January 16, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28092297/vascular-adaptations-to-habitual-exercise-in-older-adults-time-for-the-sex-talk
#20
Kerrie L Moreau, Cemal Ozemek
Regular exercise is promoted as a therapeutic strategy for age-associated endothelial dysfunction. Improvements in endothelial function are observed with endurance exercise in older men, but are diminished or absent in older women. This review examines the hypothesis that sex hormones modulate vascular adaptations to exercise training by influencing antioxidant defense systems, mitochondrial function, oxidative stress, and intracellular signaling.
January 13, 2017: Exercise and Sport Sciences Reviews
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