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Mitochondria fission

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https://www.readbyqxmd.com/read/28938192/idh2-deficiency-increases-the-liver-susceptibility-to-ischemia-reperfusion-injury-via-increased-mitochondrial-oxidative-injury
#1
Sang Jun Han, Hong Seok Choi, Jee In Kim, Jeen-Woo Park, Kwon Moo Park
Mitochondrial NADP(+)-dependent isocitrate dehydrogenase 2 (IDH2) is a major producer of mitochondrial NADPH, required for glutathione (GSH)-associated mitochondrial antioxidant systems including glutathione peroxidase (GPx) and glutathione reductase (GR). Here, we investigated the role of IDH2 in hepatic ischemia-reperfusion (HIR)-associated mitochondrial injury using Idh2-knockout (Idh2(-/-)) mice and wild-type (Idh2(+/+)) littermates. Mice were subjected to either 60min of partial liver ischemia or sham-operation...
September 8, 2017: Redox Biology
https://www.readbyqxmd.com/read/28936802/significance-of-mitochondrial-protein-post-translational-modifications-in-pathophysiology-of-brain-injury
#2
Nina Klimova, Aaron Long, Tibor Kristian
Mitochondria are complex organelles that undergo constant fusion and fission in order to adapt to the ever-changing cellular environment. The fusion/fission proteins, localized in the inner and outer mitochondrial membrane, play critical roles under pathological conditions such as acute brain injury and neurodegenerative diseases. Post-translational modifications of these proteins tightly regulate their function and activity, ultimately impacting mitochondrial dynamics and their efficiency to generate ATP. The individual post-translational modifications that are known to affect mitochondrial dynamics include SUMOylation, ubiquitination, phosphorylation, S-nitrosylation, acetylation, O-linked N-acetyl-glucosamine glycosylation, ADP-ribosylation, and proteolytic cleavage...
September 21, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/28934388/loss-of-slc25a46-causes-neurodegeneration-by-affecting-mitochondrial-dynamics-and-energy-production-in-mice
#3
Zhuo Li, Yanyan Peng, Robert B Hufnagel, Yueh-Chiang Hu, Chuntao Zhao, Luis F Queme, Zaza Khuchua, Ashley M Driver, Fei Dong, Q Richard Lu, Diana M Lindquist, Michael P Jankowski, Rolf W Stottmann, Winston W Y Kao, Taosheng Huang
Recently, we identified biallelic mutations of SLC25A46 in patients with multiple neuropathies. Functional studies revealed that SLC25A46 may play an important role in mitochondrial dynamics by mediating mitochondrial fission. However, the cellular basis and pathogenic mechanism of the SLC25A46-related neuropathies are not fully understood. Thus, we generated a Slc25a46 knock-out mouse model. Mice lacking SLC25A46 displayed severe ataxia, mainly caused by degeneration of Purkinje cells. Increased numbers of small, unmyelinated and degenerated optic nerves as well as loss of retinal ganglion cells indicated optic atrophy...
October 1, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28933354/mitochondrial-dynamics-in-mitochondrial-diseases
#4
REVIEW
Juan M Suárez-Rivero, Marina Villanueva-Paz, Patricia de la Cruz-Ojeda, Mario de la Mata, David Cotán, Manuel Oropesa-Ávila, Isabel de Lavera, Mónica Álvarez-Córdoba, Raquel Luzón-Hidalgo, José A Sánchez-Alcázar
Mitochondria are very versatile organelles in continuous fusion and fission processes in response to various cellular signals. Mitochondrial dynamics, including mitochondrial fission/fusion, movements and turnover, are essential for the mitochondrial network quality control. Alterations in mitochondrial dynamics can cause neuropathies such as Charcot-Marie-Tooth disease in which mitochondrial fusion and transport are impaired, or dominant optic atrophy which is caused by a reduced mitochondrial fusion. On the other hand, mitochondrial dysfunction in primary mitochondrial diseases promotes reactive oxygen species production that impairs its own function and dynamics, causing a continuous vicious cycle that aggravates the pathological phenotype...
December 23, 2016: Diseases (Basel)
https://www.readbyqxmd.com/read/28923365/mitochondrial-dynamics-at-the-interface-of-immune-cell-metabolism-and-function
#5
REVIEW
Angelika S Rambold, Erika L Pearce
Immune cell differentiation and function are crucially dependent on specific metabolic programs dictated by mitochondria, including the generation of ATP from the oxidation of nutrients and supplying precursors for the synthesis of macromolecules and post-translational modifications. The many processes that occur in mitochondria are intimately linked to their morphology that is shaped by opposing fusion and fission events. Exciting evidence is now emerging that demonstrates reciprocal crosstalk between mitochondrial dynamics and metabolism...
September 8, 2017: Trends in Immunology
https://www.readbyqxmd.com/read/28918113/regulation-of-mitochondrial-bioenergetics-by-the-non-canonical-roles-of-mitochondrial-dynamics-proteins-in-the-heart
#6
REVIEW
Wang Wang, Celia Fernandez-Sanz, Shey-Shing Sheu
Recent advancement in mitochondrial research has significantly extended our knowledge on the role and regulation of mitochondria in health and disease. One important breakthrough is the delineation of how mitochondrial morphological changes, termed mitochondrial dynamics, are coupled to the bioenergetics and signaling functions of mitochondria. In general, it is believed that fusion leads to an increased mitochondrial respiration efficiency and resistance to stress-induced dysfunction while fission does the contrary...
September 13, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28915614/mitochondrial-protein-18-mtp18-plays-a-pro-apoptotic-role-in-chemotherapy-induced-gastric-cancer-cell-apoptosis
#7
Lynn H H Aung, Ruibei Li, Bellur S Prabhakar, Ajay V Maker, Peifeng Li
One of the severe limitations of chemotherapy is the development of drug resistance. However, the mechanisms underlying chemotherapy resistance remain to be elucidated. Mitochondrial mediated apoptosis is a form of cell death induced by chemotherapy. Several chemotherapeutic agents have been shown to induce mitochondrial fission, and finally activate the apoptosis cascade in various cancer cells. Here, we report that the mitochondrial membrane protein 18 (MTP18) induced mitochondrial fragmentation in gastric cancer cells under doxorubicin (DOX) exposure...
August 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/28915329/mitophagy-as-a-protective-mechanism-against-myocardial-stress
#8
Jihoon Nah, Shigeki Miyamoto, Junichi Sadoshima
Mitochondria are dynamic organelles that can undergo fusion, fission, biogenesis, and autophagic elimination to maintain mitochondrial quality control. Since the heart is in constant need of high amounts of energy, mitochondria, as a central energy supply source, play a crucial role in maintaining optimal cardiac performance. Therefore, it is reasonable to assume that mitochondrial dysfunction is associated with the pathophysiology of heart diseases. In non-dividing, post-mitotic cells such as cardiomyocytes, elimination of dysfunctional organelles is essential to maintaining cellular function because non-dividing cells cannot dilute dysfunctional organelles through cell division...
September 12, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28893855/mitigating-mitochondrial-genome-erosion-without-recombination
#9
Arunas L Radzvilavicius, Hanna Kokko, Joshua R Christie
Mitochondria are ATP-producing organelles of bacterial ancestry that played a key role in the origin and early evolution of complex eukaryotic cells. Most modern eukaryotes transmit mitochondrial genes uniparentally, often without recombination among genetically divergent organelles. While this asymmetric inheritance maintains the efficacy of purifying selection at the level of the cell, the absence of recombination could also make the genome susceptible to Muller's ratchet. How mitochondria escape this irreversible defect accumulation is a fundamental unsolved question...
September 11, 2017: Genetics
https://www.readbyqxmd.com/read/28893839/mitochondrial-fission-facilitates-the-selective-mitophagy-of-protein-aggregates
#10
Jonathon L Burman, Sarah Pickles, Chunxin Wang, Shiori Sekine, Jose Norberto S Vargas, Zhe Zhang, Alice M Youle, Catherine L Nezich, Xufeng Wu, John A Hammer, Richard J Youle
Within the mitochondrial matrix, protein aggregation activates the mitochondrial unfolded protein response and PINK1-Parkin-mediated mitophagy to mitigate proteotoxicity. We explore how autophagy eliminates protein aggregates from within mitochondria and the role of mitochondrial fission in mitophagy. We show that PINK1 recruits Parkin onto mitochondrial subdomains after actinonin-induced mitochondrial proteotoxicity and that PINK1 recruits Parkin proximal to focal misfolded aggregates of the mitochondrial-localized mutant ornithine transcarbamylase (ΔOTC)...
September 11, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28891994/mdivi-1-protects-adult-rat-hippocampal-neural-stem-cells-against-palmitate-induced-oxidative-stress-and-apoptosis
#11
Sehee Kim, Chanyang Kim, Seungjoon Park
Palmitate concentrations in type 2 diabetic patients are higher than in healthy subjects. The prolonged elevation of plasma palmitate levels induces oxidative stress and mitochondrial dysfunction in neuronal cells. In this study, we examined the role of mdivi-1, a selective inhibitor of mitochondrial fission protein dynamin-regulated protein 1 (Drp1), on the survival of cultured hippocampal neural stem cells (NSCs) exposed to high palmitate. Treatment of hippocampal NSCs with mdivi-1 attenuated palmitate-induced increase in cell death and apoptosis...
September 11, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28889229/melatonin-alleviates-inflammation-induced-apoptosis-in-human-umbilical-vein-endothelial-cells-via-suppression-of-ca-2-xo-ros-drp1-mitochondrial-fission-axis-by-activation-of-ampk-serca2a-pathway
#12
Jiasen Cui, Zeng Li, Shunjiu Zhuang, Shaohong Qi, Li Li, Junwen Zhou, Wan Zhang, Yun Zhao
Endothelia inflammation damage is vital to the development and progression of chronic venous disease. In the present study, we explored the protective effect of melatonin on endothelia apoptosis induced by LPS, particularly focusing on the mitochondrial fission. We demonstrated that human umbilical vein endothelial cells (HUVEC) subjected to LPS for 12 h exhibited a higher apoptotic rate. However, melatonin (1-20 μM) treatment 12 h before LPS had the ability to protect HUVEC cell against LPS-mediated apoptosis in a dose-dependent manner...
September 9, 2017: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/28878349/peptide-mediated-delivery-of-donor-mitochondria-improves-mitochondrial-function-and-cell-viability-in-human-cybrid-cells-with-the-melas-a3243g-mutation
#13
Jui-Chih Chang, Fredrik Hoel, Ko-Hung Liu, Yau-Huei Wei, Fu-Chou Cheng, Shou-Jen Kuo, Karl Johan Tronstad, Chin-San Liu
The cell penetrating peptide, Pep-1, has been shown to facilitate cellular uptake of foreign mitochondria but further research is required to evaluate the use of Pep-1-mediated mitochondrial delivery (PMD) in treating mitochondrial defects. Presently, we sought to determine whether mitochondrial transplantation rescue mitochondrial function in a cybrid cell model of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) disease. Following PMD, recipient cells had internalized donor mitochondria after 1 h, and expressed higher levels of normal mitochondrial DNA, particularly at the end of the treatment and 11 days later...
September 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28878259/promoting-drp1-mediated-mitochondrial-fission-in-midlife-prolongs-healthy-lifespan-of-drosophila-melanogaster
#14
Anil Rana, Matheus P Oliveira, Andy V Khamoui, Ricardo Aparicio, Michael Rera, Harry B Rossiter, David W Walker
The accumulation of dysfunctional mitochondria has been implicated in aging, but a deeper understanding of mitochondrial dynamics and mitophagy during aging is missing. Here, we show that upregulating Drp1-a Dynamin-related protein that promotes mitochondrial fission-in midlife, prolongs Drosophila lifespan and healthspan. We find that short-term induction of Drp1, in midlife, is sufficient to improve organismal health and prolong lifespan, and observe a midlife shift toward a more elongated mitochondrial morphology, which is linked to the accumulation of dysfunctional mitochondria in aged flight muscle...
September 6, 2017: Nature Communications
https://www.readbyqxmd.com/read/28867389/legionella-pneumophila-modulates-mitochondrial-dynamics-to-trigger-metabolic-repurposing-of-infected-macrophages
#15
Pedro Escoll, Ok-Ryul Song, Flávia Viana, Bernhard Steiner, Thibault Lagache, Jean-Christophe Olivo-Marin, Francis Impens, Priscille Brodin, Hubert Hilbi, Carmen Buchrieser
The intracellular bacteria Legionella pneumophila encodes a type IV secretion system (T4SS) that injects effector proteins into macrophages in order to establish and replicate within the Legionella-containing vacuole (LCV). Once generated, the LCV interacts with mitochondria through unclear mechanisms. We show that Legionella uses both T4SS-independent and T4SS-dependent mechanisms to respectively interact with mitochondria and induce mitochondrial fragmentation that ultimately alters mitochondrial metabolism...
September 13, 2017: Cell Host & Microbe
https://www.readbyqxmd.com/read/28866056/mitochondrial-dynamics-transport-and-quality-control-a-bottleneck-for-retinal-ganglion-cell-viability-in-optic-neuropathies
#16
Yoko A Ito, Adriana Di Polo
Retinal ganglion cells, the neurons that selectively die in glaucoma and other optic neuropathies, are endowed with an exceedingly active metabolism and display a particular vulnerability to mitochondrial dysfunction. Mitochondria are exquisitely dynamic organelles that are continually responding to endogenous and environmental cues to readily meet the energy demand of neuronal networks. The highly orchestrated regulation of mitochondrial biogenesis, fusion, fission, transport and degradation is paramount for the maintenance of energy-expensive synapses at RGC dendrites and axon terminals geared for optimal neurotransmission...
September 1, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28860994/pioglitazone-improves-mitochondrial-function-in-the-remnant-kidney-and-protects-against-renal-fibrosis-in-5-6-nephrectomized-rats
#17
Li Sun, Quan Yuan, Tianhua Xu, Li Yao, Jiangmin Feng, Jianfei Ma, Lining Wang, Changlong Lu, Danan Wang
Pioglitazone is a type of peroxisome proliferator-activated receptor γ (PPARγ) agonist and has been demonstrated to be effective in chronic kidney diseases (CKD) treatment. However, the underlying mechanism involved in the renoprotection of pioglitazone has not been fully revealed. In the present study, the renoprotective mechanism of pioglitazone was investigated in 5/6 nephrectomized (Nx) rats and TGF-β1-exposed HK-2 cells. Pioglitazone attenuated renal injury and improved renal function, as examined by 24 h urinary protein, blood urea nitrogen and plasma creatinine in Nx rats...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28859978/carbonyl-cyanide-3-chlorophenylhydrazone-cccp-suppresses-sting-mediated-dna-sensing-pathway-through-inducing-mitochondrial-fission
#18
Dohyeong Kwon, Eunbyeol Park, Hiromi Sesaki, Suk-Jo Kang
Besides its important role in innate immune response to DNA virus infection, the regulatory function of STING in autoimmunity and cancer is emerging. Recently, multiple mechanisms regulating the activity of the STING pathway have been revealed. Previous study showed that carbonyl cyanide 3-chlorophenylhydrazone (CCCP), the protonophore, inhibited STING-mediated IFN-β production via disrupting mitochondrial membrane potential (MMP). However, how MMP dissipation leads to the suppression of the STING pathway remains unknown...
August 30, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28859443/imbalance-in-mitochondrial-dynamics-and-apoptosis-in-pregnancies-among-hiv-infected-women-on-haart-with-obstetric-complications
#19
Mariona Guitart-Mampel, A Sandra Hernandez, Constanza Moren, Marc Catalan-Garcia, Ester Tobias, Ingrid Gonzalez-Casacuberta, Diana L Juarez-Flores, Josep M Gatell, Francesc Cardellach, Jose C Milisenda, Josep M Grau, Eduard Gratacos, Francesc Figueras, Gloria Garrabou
Background: HIV infection and HAART trigger genetic and functional mitochondrial alterations leading to cell death and adverse clinical manifestations. Mitochondrial dynamics enable mitochondrial turnover and degradation of damaged mitochondria, which may lead to apoptosis. Objectives: To evaluate markers of mitochondrial dynamics and apoptosis in pregnancies among HIV-infected women on HAART and determine their potential association with obstetric complications...
September 1, 2017: Journal of Antimicrobial Chemotherapy
https://www.readbyqxmd.com/read/28842943/to-mdivi-1-or-not-to-mdivi-1-is-that-the-question
#20
REVIEW
George Smith, Gianluca Gallo
The fission/division and fusion of mitochondria are fundamental aspects of mitochondrial biology. The balance of fission and fusion sets the length of mitochondria in cells to serve their physiological requirements. The fission of mitochondria is markedly induced in many disease states and in response to cellular injury, resulting in the fragmentation of mitochondria into dysfunctional units. The mechanism that drives fission is dependent on the dynamin related protein 1 (Drp1) GTPase. mdivi-1 is a quinazolinone originally described as a selective inhibitor of Drp1, over other dynamin family members, and reported to inhibit mitochondrial fission...
August 26, 2017: Developmental Neurobiology
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