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Mitophagy

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https://www.readbyqxmd.com/read/29777261/mitochondrial-quality-control-in-amd-does-mitophagy-play-a-pivotal-role
#1
REVIEW
Juha M T Hyttinen, Johanna Viiri, Kai Kaarniranta, Janusz Błasiak
Age-related macular degeneration (AMD) is the predominant cause of visual loss in old people in the developed world, whose incidence is increasing. This disease is caused by the decrease in macular function, due to the degeneration of retinal pigment epithelium (RPE) cells. The aged retina is characterised by increased levels of reactive oxygen species (ROS), impaired autophagy, and DNA damage that are linked to AMD pathogenesis. Mitophagy, a mitochondria-specific type of autophagy, is an essential part of mitochondrial quality control, the collective mechanism responsible for this organelle's homeostasis...
May 18, 2018: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/29774638/loss-of-sirtuin-1-and-mitofusin-2-contributes-to-enhanced-ischemia-reperfusion-injury-in-aged-livers
#2
Sung Kook Chun, Sooyeon Lee, Joseph Flores-Toro, Rebecca Y U, Ming-Jim Yang, Kristina L Go, Thomas G Biel, Catherine E Miney, Schiley Pierre Louis, Brian K Law, Mary E Law, Elizabeth M Thomas, Kevin E Behrns, Christiaan Leeuwenburgh, Jae-Sung Kim
Ischemia/reperfusion (I/R) injury is a causative factor contributing to morbidity and mortality during liver resection and transplantation. Livers from elderly patients have a poorer recovery from these surgeries, indicating reduced reparative capacity with aging. Mechanisms underlying this age-mediated hypersensitivity to I/R injury remain poorly understood. Here, we investigated how sirtuin 1 (SIRT1) and mitofusin 2 (MFN2) are affected by I/R in aged livers. Young (3 months) and old (23-26 months) male C57/BL6 mice were subjected to hepatic I/R in vivo...
May 17, 2018: Aging Cell
https://www.readbyqxmd.com/read/29767769/regulation-of-chlorophagy-during-photoinhibition-and-senescence-lessons-from-mitophagy
#3
Sakuya Nakamura, Masanori Izumi
Light energy is essential for photosynthetic energy production and plant growth. Chloroplasts in green tissues convert energy from sunlight into chemical energy via the electron transport chain. When the level of light energy exceeds the capacity of the photosynthetic apparatus, chloroplasts undergo a process known as photoinhibition. Since photoinhibition leads to the overaccumulation of reactive oxygen species (ROS) and the spreading of cell death, plants have developed multiple systems to protect chloroplasts from strong light...
May 14, 2018: Plant & Cell Physiology
https://www.readbyqxmd.com/read/29764564/mitochondria-mediated-defense-mechanisms-against-pathogens-in-caenorhabditis-elegans
#4
Sujeong Kwon, Eun Ji E Kim, Seung-Jae V Lee
Mitochondria are crucial organelles that generate cellular energy and metabolites. Recent studies indicate that mitochondria also regulate immunity. In this review, we discuss key roles of mitochondria in immunity against pathogen infection and underlying mechanisms, focusing on discoveries using Caenorhabditis elegans. Various mitochondrial processes, including mitochondrial surveillance mechanisms, mitochondrial unfolded protein response (UPRmt), mitophagy, and reactive oxygen species (ROS) production, contribute to immune responses and resistance of C...
May 16, 2018: BMB Reports
https://www.readbyqxmd.com/read/29755319/ambra1-mediated-mitophagy-counteracts-oxidative-stress-and-apoptosis-induced-by-neurotoxicity-in-human-neuroblastoma-sh-sy5y-cells
#5
Anthea Di Rita, Pasquale D'Acunzo, Luca Simula, Silvia Campello, Flavie Strappazzon, Francesco Cecconi
Therapeutic strategies are needed to protect dopaminergic neurons in Parkinson's disease (PD) patients. Oxidative stress caused by dopamine may play an important role in PD pathogenesis. Selective autophagy of mitochondria (mitophagy), mainly regulated by PINK1 and PARKIN, plays an important role in the maintenance of cell homeostasis. Mutations in those genes cause accumulation of damaged mitochondria, leading to nigral degeneration and early-onset PD. AMBRA1ActA is a fusion protein specifically expressed at the mitochondria, and whose expression has been shown to induce a powerful mitophagy in mammalian cells...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29749796/nuclear-tp53-an-unraveled-function-as-transcriptional-repressor-of-pink1
#6
Frédéric Checler, Thomas Goiran, Cristine Alves da Costa
The tumor suppressor TP53/p53 is a key protein in both neurodegenerative diseases and cancer. Thus, TP53-linked cell death appears exacerbated in several age-related neuropathologies, while TP53 mutation-associated phenotypes indicate a loss of function accounting for approximately half of cancers. Thus, TP53 plays a pivotal role in these phenotypically distinct pathologies, a hypothesis reinforced by recent epidemiological studies suggesting an opposite risk to develop one type of pathology relative to the other...
May 11, 2018: Autophagy
https://www.readbyqxmd.com/read/29749586/porcine-cell-free-system-to-study-mammalian-sperm-mitophagy
#7
Won-Hee Song, Peter Sutovsky
A cell-free system using oocyte extracts is a valuable tool to study early events of animal fertilization and examine protein-protein interactions difficult to observe in whole cells. The process of postfertilization sperm mitophagy assures timely elimination of paternal, sperm-contributed mitochondria carrying potentially corrupted mitochondrial DNA (mtDNA). Cell-free systems would be especially advantageous for studying postfertilization sperm mitophagy as large amounts of oocyte extracts can be incubated with hundreds to thousands of spermatozoa in a single trial, while only one spermatozoon per zygote can be examined by whole-cell approaches...
May 11, 2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29746779/energy-metabolism-drugs-block-triple-negative-breast-metastatic-cancer-cell-phenotype
#8
Silvia Cecilia Pacheco-Velazquez, Diana Xochiquetzal Robledo-Cadena, Ileana Hernández-Reséndiz, Juan Carlos Gallardo-Pérez, Rafael Moreno-Sánchez, Sara Rodríguez-Enríquez
To establish alternative targeted therapies against triple negative (TN) breast cancer, (1) the energy metabolism and (2) the sensitivity of cell growth, migration and invasiveness towards metabolic, canonical and NSAID inhibitors was analyzed in MDA-MB-231 and MDA-MB-468, two TN metastatic breast cancer cell lines, under both normoxia (21% O2) and hypoxia (0.1% O2). For comparative purposes, analysis was also carried out in the less-metastatic breast MCF-7 cancer cells. Under normoxia, oxidative phosphorylation (OxPhos) was significantly higher (2-times) in MDA-MB-468 than in MDA-MB-231 and MCF-7 whereas their glycolytic fluxes and OxPhos and glycolytic protein contents were all similar...
May 10, 2018: Molecular Pharmaceutics
https://www.readbyqxmd.com/read/29744594/nr4a1-aggravates-the-cardiac-microvascular-ischemia-reperfusion-injury-through-suppressing-fundc1-mediated-mitophagy-and-promoting-mff-required-mitochondrial-fission-by-ck2%C3%AE
#9
Hao Zhou, Jin Wang, Pingjun Zhu, Hong Zhu, Sam Toan, Shunying Hu, Jun Ren, Yundai Chen
Mitochondrial fission and mitophagy are considered key processes involved in the pathogenesis of cardiac microvascular ischemia reperfusion (IR) injury although the upstream regulatory mechanism for fission and mitophagy still remains unclear. Herein, we reported that NR4A1 was significantly upregulated following cardiac microvascular IR injury, and its level was positively correlated with microvascular collapse, endothelial cellular apoptosis and mitochondrial damage. However, NR4A1-knockout mice exhibited resistance against the acute microvascular injury and mitochondrial dysfunction compared with the wild-type mice...
May 9, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29744294/synergistic-effects-of-hmg-coa-reductase-inhibitor-and-angiotensin-ii-receptor-blocker-on-load-induced-heart-failure
#10
Yusuke Ito, Yasuhiro Maejima, Natsuko Tamura, Yuka Shiheido-Watanabe, Masanori Konishi, Takashi Ashikaga, Kenzo Hirao, Mitsuaki Isobe
5-Hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins) have beneficial effects in patients with heart failure (HF), regardless of serum cholesterol levels. However, their synergic effects with angiotensin II receptor blocker (ARB) remain to be established. We assessed the existence and potential underlying mechanisms of the effects of combined ARB [losartan (LOS)] and statin [simvastatin (SIM)] on cardiac function in rats and mice with load-induced HF. Salt-loaded Dahl salt-sensitive (DS) rats were treated with vehicle, LOS, SIM, or LOS + SIM for 8 weeks...
May 2018: FEBS Open Bio
https://www.readbyqxmd.com/read/29743550/inhibitor-of-apoptosis-proteins-are-required-for-effective-fusion-of-autophagosomes-with-lysosomes
#11
Sylwia Gradzka, Oliver S Thomas, Oliver Kretz, Aladin Haimovici, Lazaros Vasilikos, Wendy Wei-Lynn Wong, Georg Häcker, Ian E Gentle
Inhibitor of Apoptosis Proteins act as E3 ubiquitin ligases to regulate NF-κB signalling from multiple pattern recognition receptors including NOD2, as well as TNF Receptor Superfamily members. Loss of XIAP in humans causes X-linked Lymphoproliferative disease type 2 (XLP-2) and is often associated with Crohn's disease. Crohn's disease is also caused by mutations in the gene encoding NOD2 but the mechanisms behind Crohn's disease development in XIAP and NOD2 deficient-patients are still unknown. Numerous other mutations causing Crohn's Disease occur in genes controlling various aspects of autophagy, suggesting a strong involvement of autophagy in preventing Crohn's disease...
May 9, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29732060/multicolor-monitoring-of-cellular-organelles-by-single-wavelength-excitation-to-visualize-the-mitophagy-process
#12
Fang Hu, Xiaolei Cai, Purnima Naresh Manghnani, Kenry, Wenbo Wu, Bin Liu
Multiplexed cellular organelle imaging using single wavelength excitation is highly desirable for unravelling cellular functions but remains challenging. This requires the design of organelle specific fluorophores with distinct emission but similar absorption. Herein, we present two unique aggregation-induced emission (AIE) probes to track mitochondria and lysosomes simultaneously with emission colors that can be distinguished from that of the nucleus stain Hoechst 33342 upon single wavelength excitation. Compared to conventional organelle stains, the two AIE probes have larger Stokes shifts and higher photostability, which endow them with the capability to monitor bioprocesses, such as mitophagy with strong and sustained fluorescent signals...
March 14, 2018: Chemical Science
https://www.readbyqxmd.com/read/29729358/doxorubicin-induced-mitophagy-and-mitochondrial-damage-is-associated-with-dysregulation-of-the-pink1-parkin-pathway
#13
Jian Yin, Jiabin Guo, Qiang Zhang, Lan Cui, Li Zhang, Tingfen Zhang, Jun Zhao, Jin Li, Alistair Middleton, Paul L Carmichael, Shuangqing Peng
The usefulness of doxorubicin (DOX), a potent anticancer agent, is limited by its cardiotoxicity. Mitochondria play a central role in DOX-induced cardiotoxicity though the precise mechanisms are still obscure. Increasing evidence indicates that excessive activation of mitophagy and mitochondrial dysfunction are key causal events leading to DOX-induced cardiac injury. The PINK1/parkin pathway has emerged as a critical pathway in regulation of mitophagy as well as mitochondrial function. The present study was aimed to investigate the role of PINK1/parkin pathway in DOX-induced mitochondrial damage and cardiotoxicity...
May 3, 2018: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/29723606/salidroside-mediated-stabilization-of-bcl-x-l-prevents-mitophagy-in-ca3-hippocampal-neurons-during-hypoxia
#14
Suryanarayan Biswal, Kalpana Kumari Barhwal, Debashree Das, Richa Dhingra, Nilima Dhingra, Tapas Chanda Nag, Sunil Kumar Hota
Chronic hypoxic stress results in deposition of lipofuscin granules in the CA3 region of hippocampal neurons which contributes to neurodegeneration and accelerated neuronal aging. Oxidative stress and mitophagy during hypoxia are crucial to cause aggregation of these lipofuscin granules in hypoxic neurons. Salidroside, a glucoside derivative of β-Tyrosol, has been reported to protect hypoxic neurons through maintenance of mitochondrial activity. The present study is aimed at investigating the potential of Salidroside in preventing mitophagy during chronic hypoxia and identification of the molecular targets and underlying signaling mechanisms...
April 30, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29721922/mitochondria-potential-targets-for-protection-in-age-related-macular-degeneration
#15
Emily E Brown, Alfred S Lewin, John D Ash
Age-related macular degeneration (AMD) is the leading cause of blindness in older adults in developed countries. The molecular mechanisms of disease pathogenesis remain poorly understood; however, evidence suggests that mitochondrial dysfunction may contribute to the progression of the disease. Studies have shown that mitochondrial DNA lesions are increased in the retinal pigment epithelium (RPE) of human patients with the disease and that the number of these lesions increases with disease severity. Additionally, microscopy of human RPE from patients with dry AMD shows severe disruptions in mitochondrial inner and outer membrane structure, mitochondrial size, and mitochondrial cellular organization...
2018: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29719250/mitophagy-directs-muscle-adipose-crosstalk-to-alleviate-dietary-obesity
#16
Tingting Fu, Zhisheng Xu, Lin Liu, Qiqi Guo, Hao Wu, Xijun Liang, Danxia Zhou, Liwei Xiao, Lei Liu, Yong Liu, Min-Sheng Zhu, Quan Chen, Zhenji Gan
The quality of mitochondria in skeletal muscle is essential for maintaining metabolic homeostasis during adaptive stress responses. However, the precise control mechanism of muscle mitochondrial quality and its physiological impacts remain unclear. Here, we demonstrate that FUNDC1, a mediator of mitophagy, plays a critical role in controlling muscle mitochondrial quality as well as metabolic homeostasis. Skeletal-muscle-specific ablation of FUNDC1 in mice resulted in LC3-mediated mitophagy defect, leading to impaired mitochondrial energetics...
May 1, 2018: Cell Reports
https://www.readbyqxmd.com/read/29718288/the-pathogenesis-of-lysosomal-storage-disorders-beyond-the-engorgement-of-lysosomes-to-abnormal-development-and-neuroinflammation
#17
Maria Teresa Fiorenza, Enrico Moro, Robert P Erickson
There is growing evidence that the complex clinical manifestations of lysosomal storage diseases (LSDs) are not fully explained by the engorgement of the endosomal-autophagic-lysosomal system. In this review, we explore current knowledge of common pathogenetic mechanisms responsible for the early onset of tissue abnormalities of two LSDs, Mucopolysaccharidosis type II (MPSII) and Niemann-Pick type C (NPC) diseases. In particular, perturbations of the homeostasis of glycosaminoglycans (GAGs) and cholesterol (Chol) in MPSII and NPC diseases, respectively, affect key biological processes, including morphogen signaling...
April 28, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29715546/tdp-43-interacts-with-mitochondrial-proteins-critical-for-mitophagy-and-mitochondrial-dynamics
#18
Stephani A Davis, Sheed Itaman, Christopher M Khalid-Janney, Justin A Sherard, James A Dowell, Nigel J Cairns, Michael A Gitcho
Transactive response DNA-binding protein of 43 kDa (TDP-43) functions as a heterogeneous nuclear ribonucleoprotein and is the major pathological protein in frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis/motor neuron disease (ALS/MND). TDP-43 pathology may also be present as a comorbidity in approximately 20-50% of sporadic Alzheimer's disease cases. In a mouse model of MND, full-length TDP-43 increases association with the mitochondria and blocking the TDP-43/mitochondria interaction ameliorates motor dysfunction...
April 30, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29708514/systemic-isradipine-treatment-diminishes-calcium-dependent-mitochondrial-oxidant-stress
#19
Jaime N Guzman, Ema Ilijic, Ben Yang, Javier Sanchez-Padilla, David Wokosin, Dan Galtieri, Jyothisri Kondapalli, Paul T Schumacker, D James Surmeier
The ability of the Cav1 channel inhibitor isradipine to slow the loss of substantia nigra pars compacta (SNc) dopaminergic (DA) neurons and the progression of Parkinson's disease (PD) is being tested in a phase 3 human clinical trial. But it is unclear whether and how chronic isradipine treatment will benefit SNc DA neurons in vivo. To pursue this question, isradipine was given systemically to mice at doses that achieved low nanomolar concentrations in plasma, near those achieved in patients. This treatment diminished cytosolic Ca2+ oscillations in SNc DA neurons without altering autonomous spiking or expression of Ca2+ channels, an effect mimicked by selectively knocking down expression of Cav1...
April 30, 2018: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29705815/pancreatic-%C3%AE-cells-overexpressing-hiapp-impaired-mitophagy-and-unbalanced-mitochondrial-dynamics
#20
Miriam García Hernández, Ana García Aguilar, Jesús Burillo, Raquel Gómez Oca, Maria Antonietta Manca, Ana Novials, Gema Alcarraz-Vizan, Carlos Guillén, Manuel Benito
Human islet amyloid polypeptide (hIAPP), or amylin, has the tendency to aggregate into insoluble amyloid fibrils, a typical feature of islets from type 2 diabetes individuals. Thus, we investigated comparatively the impact of hIAPP on key pathways involved in pancreatic beta survival. INS1E-hIAPP cells present a hyperactivation of MTORC1 and an inhibition of autophagy signaling, those cells showing an increase in cell size. Resveratrol, a MTORC1 inhibitor, can reverse TSC2 degradation that occurs in INS1E-hIAPP cells and diminished MTORC1 hyperactivation with concomitant autophagy stimulation...
April 29, 2018: Cell Death & Disease
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