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Mitochondrial fission

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https://www.readbyqxmd.com/read/28944094/the-arl2-gtpase-regulates-mitochondrial-fusion-from-the-intermembrane-space
#1
Laura E Newman, Cara R Schiavon, Rachel E Turn, Richard A Kahn
Mitochondria are essential, dynamic organelles that regularly undergo both fusion and fission in response to cellular conditions, though mechanisms of the regulation of their dynamics are incompletely understood. We provide evidence that increased activity of the small GTPase ARL2 is strongly correlated with an increase in fusion, while loss of ARL2 activity results in a decreased rate of mitochondrial fusion. Strikingly, expression of activated ARL2 can partially restore the loss of fusion resulting from deletion of either mitofusin 1 (MFN1) or mitofusin 2 (MFN2), but not deletion of both...
2017: Cellular Logistics
https://www.readbyqxmd.com/read/28942921/mitochondrial-fission-promotes-the-continued-clearance-of-apoptotic-cells-by-macrophages
#2
Ying Wang, Manikandan Subramanian, Arif Yurdagul, Valéria C Barbosa-Lorenzi, Bishuang Cai, Jaime de Juan-Sanz, Timothy A Ryan, Masatoshi Nomura, Frederick R Maxfield, Ira Tabas
Clearance of apoptotic cells (ACs) by phagocytes (efferocytosis) prevents post-apoptotic necrosis and dampens inflammation. Defective efferocytosis drives important diseases, including atherosclerosis. For efficient efferocytosis, phagocytes must be able to internalize multiple ACs. We show here that uptake of multiple ACs by macrophages requires dynamin-related protein 1 (Drp1)-mediated mitochondrial fission, which is triggered by AC uptake. When mitochondrial fission is disabled, AC-induced increase in cytosolic calcium is blunted owing to mitochondrial calcium sequestration, and calcium-dependent phagosome formation around secondarily encountered ACs is impaired...
September 20, 2017: Cell
https://www.readbyqxmd.com/read/28942427/binding-of-fundc1-with-inositol-1-4-5-trisphosphate-receptor-in-mitochondria-associated-endoplasmic-reticulum-er-membranes-maintains-mitochondrial-dynamics-and-function-in-hearts-in-vivo
#3
Shengnan Wu, Qiulun Lu, Qilong Wang, Ye Ding, Zejun Ma, Xiaoxiang Mao, Kai Huang, Zhonglin Xie, Ming-Hui Zou
Background -FUN14 domain containing 1 (FUNDC1) is a highly conserved outer mitochondrial membrane protein. The aim of this study is to examine if FUNDC1 modulates the mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs), mitochondrial morphology, and function in cardiomyocytes and in intact hearts. Methods -The impacts of FUNDC1 on MAMs formation and cardiac functions were studied in mouse neonatal cardiomyocytes, in mice with cardiomyocyte-specific Fundc1 gene knockout (Fundc1(f/Y)/Cre(αMyHC+/-) ), and in the cardiac tissues of the patients with heart failure...
September 23, 2017: Circulation
https://www.readbyqxmd.com/read/28941171/roles-of-mitochondrial-dynamics-modulators-in-cardiac-ischaemia-reperfusion-injury
#4
REVIEW
Chayodom Maneechote, Siripong Palee, Siriporn C Chattipakorn, Nipon Chattipakorn
The current therapeutic strategy for the management of acute myocardial infarction (AMI) is to return blood flow into the occluded coronary artery of the heart, a process defined as reperfusion. However, reperfusion itself can increase mortality rates in AMI patients because of cardiac tissue damage and dysfunction, which is termed 'ischaemia/reperfusion (I/R) injury'. Mitochondria play an important role in myocardial I/R injury as disturbance of mitochondrial dynamics, especially excessive mitochondrial fission, is a predominant cause of cardiac dysfunction...
September 22, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28939434/inhibition-of-drp1-mediated-mitochondrial-fission-improves-mitochondrial-dynamics-and-bioenergetics-stimulating-neurogenesis-in-hippocampal-progenitor-cells-from-a-down-syndrome-mouse-model
#5
Daniela Valenti, Leonardo Rossi, Domenico Marzulli, Francesco Bellomo, Domenico De Rasmo, Anna Signorile, Rosa Anna Vacca
Functional and structural damages to mitochondria have been critically associated with the pathogenesis of Down syndrome (DS), a human multifactorial disease caused by trisomy of chromosome 21 and associated with neurodevelopmental delay, intellectual disability and early neurodegeneration. Recently, we demonstrated in neural progenitor cells (NPCs) isolated from the hippocampus of Ts65Dn mice -a widely used model of DS - a severe impairment of mitochondrial bioenergetics and biogenesis and reduced NPC proliferation...
September 19, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28938192/idh2-deficiency-increases-the-liver-susceptibility-to-ischemia-reperfusion-injury-via-increased-mitochondrial-oxidative-injury
#6
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
#7
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
#8
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
#9
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
#10
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/28919853/p47phox-cdk5-drp1-mediated-mitochondrial-fission-evokes-pv-cell-degeneration-in-the-rat-dentate-gyrus-following-status-epilepticus
#11
Ji-Eun Kim, Tae-Cheon Kang
Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mechanism remains to be clarified. In the present study, we found that p47Phox expression was transiently and selectively increased in PV neurons 6 h after SE. This up-regulated p47Phox expression was accompanied by excessive mitochondrial fission...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28918902/mtor-controls-mitochondrial-dynamics-and-cell-survival-via-mtfp1
#12
Masahiro Morita, Julien Prudent, Kaustuv Basu, Vanessa Goyon, Sakie Katsumura, Laura Hulea, Dana Pearl, Nadeem Siddiqui, Stefan Strack, Shawn McGuirk, Julie St-Pierre, Ola Larsson, Ivan Topisirovic, Hojatollah Vali, Heidi M McBride, John J Bergeron, Nahum Sonenberg
The mechanisms that link environmental and intracellular stimuli to mitochondrial functions, including fission/fusion, ATP production, metabolite biogenesis, and apoptosis, are not well understood. Here, we demonstrate that the nutrient-sensing mechanistic/mammalian target of rapamycin complex 1 (mTORC1) stimulates translation of mitochondrial fission process 1 (MTFP1) to control mitochondrial fission and apoptosis. Expression of MTFP1 is coupled to pro-fission phosphorylation and mitochondrial recruitment of the fission GTPase dynamin-related protein 1 (DRP1)...
September 21, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28918113/regulation-of-mitochondrial-bioenergetics-by-the-non-canonical-roles-of-mitochondrial-dynamics-proteins-in-the-heart
#13
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
#14
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
#15
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/28913665/role-of-noncoding-rnas-in-regulation-of-cardiac-cell-death-and-cardiovascular-diseases
#16
REVIEW
Yanhan Dong, Cuiyun Liu, Yanfang Zhao, Murugavel Ponnusamy, Peifeng Li, Kun Wang
Loss of functional cardiomyocytes is a major underlying mechanism for myocardial remodeling and heart diseases, due to the limited regenerative capacity of adult myocardium. Apoptosis, programmed necrosis, and autophagy contribute to loss of cardiac myocytes that control the balance of cardiac cell death and cell survival through multiple intricate signaling pathways. In recent years, non-coding RNAs (ncRNAs) have received much attention to uncover their roles in cell death of cardiovascular diseases, such as myocardial infarction, cardiac hypertrophy, and heart failure...
September 14, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28893855/mitigating-mitochondrial-genome-erosion-without-recombination
#17
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
#18
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
#19
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
#20
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
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