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https://www.readbyqxmd.com/read/29107116/mitophagy-and-the-release-of-inflammatory-cytokines
#1
REVIEW
James Harris, Nadia Deen, Shahrzad Zamani, Md Abul Hasnat
Mitophagy is a selective form of autophagy in which damaged or dysfunctional mitochondria are specifically targeted by autophagosomes for lysosomal degradation. Studies have demonstrated that loss of autophagy/mitophagy can lead to a build-up of cytosolic reactive oxygen species and mitochondrial DNA, which can, in turn, activate immune signalling pathways that ultimately lead to the releases of inflammatory cytokines, including IL-1α, IL-1β, IL-18 and macrophage migration inhibitory factor (MIF). Moreover, release of these cytokines can subsequently promote the release of others, including IL-23 and IL-17...
October 26, 2017: Mitochondrion
https://www.readbyqxmd.com/read/29077752/isg15-governs-mitochondrial-function-in-macrophages-following-vaccinia-virus-infection
#2
Sara Baldanta, Mercedes Fernández-Escobar, Rebeca Acín-Perez, Manuel Albert, Emilio Camafeita, Inmaculada Jorge, Jesús Vázquez, José Antonio Enríquez, Susana Guerra
The interferon (IFN)-stimulated gene 15 (ISG15) encodes one of the most abundant proteins induced by interferon, and its expression is associated with antiviral immunity. To identify protein components implicated in IFN and ISG15 signaling, we compared the proteomes of ISG15-/- and ISG15+/+ bone marrow derived macrophages (BMDM) after vaccinia virus (VACV) infection. The results of this analysis revealed that mitochondrial dysfunction and oxidative phosphorylation (OXPHOS) were pathways altered in ISG15-/- BMDM treated with IFN...
October 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/29054471/innate-immunity-and-tolerance-toward-mitochondria
#3
REVIEW
Anthony Rongvaux
Mitochondria are intracellular organelles that originate from a bacterial symbiont, and they retain multiple features of this bacterial ancestry. The immune system evolved to detect the presence of invading pathogens, including bacteria, to eliminate them by a diversity of antimicrobial mechanisms and to mount long-term protective immunity. Due to their bacterial ancestry, mitochondria are sensed by the innate immune system, and trigger inflammatory responses comparable to those induced by pathogenic bacteria...
October 17, 2017: Mitochondrion
https://www.readbyqxmd.com/read/29049365/myd88-dependent-inflammasome-activation-and-autophagy-inhibition-contributes-to-ehrlichia-induced-liver-injury-and-toxic-shock
#4
Muhamuda Kader, Mounia Alaoui-El-Azher, Jennie Vorhauer, Bhushan B Kode, Jakob Z Wells, Donna Stolz, George Michalopoulos, Alan Wells, Melanie Scott, Nahed Ismail
Severe hepatic inflammation is a common cause of acute liver injury following systemic infection with Ehrlichia, obligate Gram-negative intracellular bacteria that lack lipopolysaccharide (LPS). We have previously shown that type I IFN (IFN-I) and inflammasome activation are key host-pathogenic mediators that promote excessive inflammation and liver damage following fatal Ehrlichia infection. However, the underlying signals and mechanisms that regulate protective immunity and immunopathology during Ehrlichia infection are not well understood...
October 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28978702/coxsackievirus-b-escapes-the-infected-cell-in-ejected-mitophagosomes
#5
Jon Sin, Laura McIntyre, Aleksandr Stotland, Ralph Feuer, Roberta A Gottlieb
Coxsackievirus B (CVB) is a common enterovirus that can cause various systemic inflammatory diseases. Because CVB lacks an envelope, it has been thought to be inherently cytolytic, wherein CVB can escape from the infected host cell only by causing it to rupture. In recent years, however, we and others have observed that various naked viruses, such as CVB, can trigger the release of infectious extracellular microvesicles (EMVs) that contain viral material. This mode of cellular escape has been suggested to allow the virus to be masked from the adaptive immune system...
December 15, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28768533/progression-of-pathology-in-pink1-deficient-mouse-brain-from-splicing-via-ubiquitination-er-stress-and-mitophagy-changes-to-neuroinflammation
#6
Sylvia Torres-Odio, Jana Key, Hans-Hermann Hoepken, Júlia Canet-Pons, Lucie Valek, Bastian Roller, Michael Walter, Blas Morales-Gordo, David Meierhofer, Patrick N Harter, Michel Mittelbronn, Irmgard Tegeder, Suzana Gispert, Georg Auburger
BACKGROUND: PINK1 deficiency causes the autosomal recessive PARK6 variant of Parkinson's disease. PINK1 activates ubiquitin by phosphorylation and cooperates with the downstream ubiquitin ligase PARKIN, to exert quality control and control autophagic degradation of mitochondria and of misfolded proteins in all cell types. METHODS: Global transcriptome profiling of mouse brain and neuron cultures were assessed in protein-protein interaction diagrams and by pathway enrichment algorithms...
August 2, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28747873/mitochondria-bioenergetics-and-excitotoxicity-new-therapeutic-targets-in-perinatal-brain-injury
#7
REVIEW
Bryan Leaw, Syam Nair, Rebecca Lim, Claire Thornton, Carina Mallard, Henrik Hagberg
Injury to the fragile immature brain is implicated in the manifestation of long-term neurological disorders, including childhood disability such as cerebral palsy, learning disability and behavioral disorders. Advancements in perinatal practice and improved care mean the majority of infants suffering from perinatal brain injury will survive, with many subtle clinical symptoms going undiagnosed until later in life. Hypoxic-ischemia is the dominant cause of perinatal brain injury, and constitutes a significant socioeconomic burden to both developed and developing countries...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28668382/inflammation-and-mitochondrial-dysfunction-a-vicious-circle-in-neurodegenerative-disorders
#8
REVIEW
Jack van Horssen, Pauline van Schaik, Maarten Witte
Experimental evidence supports an intricate association between inflammation and mitochondrial dysfunction as main contributors of neurological diseases. Inflammatory mediators produced by activated microglia and infiltrated immune cells trigger intracellular signaling cascades that can alter cellular mitochondrial metabolism. Cytokines, particularly tumor necrosis factor-alpha, impede mitochondrial oxidative phosphorylation and associated ATP production and instigate mitochondrial reactive oxygen species production...
June 28, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28663335/mitochondrial-quality-control-in-alveolar-epithelial-cells-damaged-by-s-aureus-pneumonia-in-mice
#9
Hagir B Suliman, Bryan Kraft, Raquel Bartz, Lingye Chen, Karen E Welty-Wolf, Claude A Piantadosi
Mitochondrial damage is often overlooked in acute lung injury (ALI), yet most of the lung's physiological processes, such as airway tone, mucociliary clearance, ventilation-perfusion (Va/Q) matching, and immune surveillance require aerobic energy provision. Because the cell's mitochondrial quality control (QC) process regulates the elimination and replacement of damaged mitochondria to maintain cell survival, we serially evaluated mitochondrial biogenesis and mitophagy in the alveolar regions of mice in a validated Staphylococcus aureus pneumonia model...
October 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28615325/calcium-calmodulin-dependent-protein-kinase-regulates-the-pink1-parkin-and-dj-1-pathways-of-mitophagy-during-sepsis
#10
Xianghong Zhang, Du Yuan, Qian Sun, Li Xu, Emma Lee, Anthony J Lewis, Brian S Zuckerbraun, Matthew R Rosengart
During sepsis and shock states, mitochondrial dysfunction occurs. Consequently, adaptive mechanisms, such as fission, fusion, and mitophagy, are induced to eliminate damaged portions or entire dysfunctional mitochondria. The regulatory PINK1/Parkin and DJ-1 pathways are strongly induced by mitochondrial depolarization, although a direct link between loss of mitochondrial membrane potential (ΔΨ) and mitophagy has not been identified. Mitochondria also buffer Ca(2+), and their buffering capacity is dependent on ΔΨ Here, we characterize a role for calcium/calmodulin-dependent protein kinase (CaMK) I in the regulation of these mechanisms...
October 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28607490/multiple-truncated-isoforms-of-mavs-prevent-its-spontaneous-aggregation-in-antiviral-innate-immune-signalling
#11
Nan Qi, Yuheng Shi, Rui Zhang, Wenting Zhu, Bofeng Yuan, Xiaoyan Li, Changwan Wang, Xuewu Zhang, Fajian Hou
In response to virus infection, RIG-I-like receptors (RLRs) sense virus RNA and induce MAVS to form prion-like aggregates to further propagate antiviral signalling. Although monomeric MAVS recombinant protein can assemble into prion-like filaments spontaneously in vitro, endogenous MAVS in cells is prevented from aggregation until viral infection. The mechanism preventing cellular MAVS from spontaneous aggregation is unclear. Here we show that multiple N-terminal truncated isoforms of MAVS are essential in preventing full-length MAVS from spontaneous aggregation through transmembrane domain-mediated homotypic interaction...
June 13, 2017: Nature Communications
https://www.readbyqxmd.com/read/28539244/manganese-exposure-induces-neuroinflammation-by-impairing-mitochondrial-dynamics-in-astrocytes
#12
Souvarish Sarkar, Emir Malovic, Dilshan S Harischandra, Hilary A Ngwa, Anamitra Ghosh, Colleen Hogan, Dharmin Rokad, Gary Zenitsky, Huajun Jin, Vellareddy Anantharam, Anumantha G Kanthasamy, Arthi Kanthasamy
Chronic manganese (Mn) exposure induces neurotoxicity, which is characterized by Parkinsonian symptoms resulting from impairment in the extrapyramidal motor system of the basal ganglia. Mitochondrial dysfunction and oxidative stress are considered key pathophysiological features of Mn neurotoxicity. Recent evidence suggests astrocytes as a major target of Mn neurotoxicity since Mn accumulates predominantly in astrocytes. However, the primary mechanisms underlying Mn-induced astroglial dysfunction and its role in metal neurotoxicity are not completely understood...
May 21, 2017: Neurotoxicology
https://www.readbyqxmd.com/read/28507507/pink1-parkin-dependent-mitochondrial-surveillance-from-pleiotropy-to-parkinson-s-disease
#13
REVIEW
Francois Mouton-Liger, Maxime Jacoupy, Jean-Christophe Corvol, Olga Corti
Parkinson's disease (PD) is one of the most frequent neurodegenerative disease caused by the preferential, progressive degeneration of the dopaminergic (DA) neurons of the substantia nigra (SN) pars compacta. PD is characterized by a multifaceted pathological process involving protein misfolding, mitochondrial dysfunction, neuroinflammation and metabolism deregulation. The molecular mechanisms governing the complex interplay between the different facets of this process are still unknown. PARK2/Parkin and PARK6/PINK1, two genes responsible for familial forms of PD, act as a ubiquitous core signaling pathway, coupling mitochondrial stress to mitochondrial surveillance, by regulating mitochondrial dynamics, the removal of damaged mitochondrial components by mitochondria-derived vesicles, mitophagy, and mitochondrial biogenesis...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28473584/anti-inflammatory-effect-of-il-10-mediated-by-metabolic-reprogramming-of-macrophages
#14
W K Eddie Ip, Namiko Hoshi, Dror S Shouval, Scott Snapper, Ruslan Medzhitov
Interleukin 10 (IL-10) is an anti-inflammatory cytokine that plays a critical role in the control of immune responses. However, its mechanisms of action remain poorly understood. Here, we show that IL-10 opposes the switch to the metabolic program induced by inflammatory stimuli in macrophages. Specifically, we show that IL-10 inhibits lipopolysaccharide-induced glucose uptake and glycolysis and promotes oxidative phosphorylation. Furthermore, IL-10 suppresses mammalian target of rapamycin (mTOR) activity through the induction of an mTOR inhibitor, DDIT4...
May 5, 2017: Science
https://www.readbyqxmd.com/read/28456642/pathophysiology-of-mitochondrial-lipid-oxidation-role-of-4-hydroxynonenal-4-hne-and-other-bioactive-lipids-in-mitochondria
#15
REVIEW
Mengqing Xiao, Huiqin Zhong, Lin Xia, Yongzhen Tao, Huiyong Yin
Mitochondrial lipids are essential for maintaining the integrity of mitochondrial membranes and the proper functions of mitochondria. As the "powerhouse" of a cell, mitochondria are also the major cellular source of reactive oxygen species (ROS). Oxidative stress occurs when the antioxidant system is overwhelmed by overproduction of ROS. Polyunsaturated fatty acids in mitochondrial membranes are primary targets for ROS attack, which may lead to lipid peroxidation (LPO) and generation of reactive lipids, such as 4-hydroxynonenal...
October 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28366813/mita-modulated-autophagy-flux-promotes-cell-death-in-breast-cancer-cells
#16
Khyati Bhatelia, Kritarth Singh, Paresh Prajapati, Lakshmi Sripada, Milton Roy, Rajesh Singh
The crosstalk between inflammation and autophagy is an emerging phenomenon observed during tumorigenesis. Activation of NF-κB and IRF3 plays a key role in the regulation of cytokines that are involved in tumor growth and progression. The genes of innate immunity are known to regulate the master transcription factors like NF-κB and IRF3. Innate immunity pathways at the same time regulate the genes of the autophagy pathway which are essential for tumor cell metabolism. In the current study, we studied the role of MITA (Mediator of IRF3 Activation), a regulator of innate immunity, in the regulation of autophagy and its implication in cell death of breast cancer cells...
March 31, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28331061/an-intracellular-matrix-metalloproteinase-2-isoform-induces-tubular-regulated-necrosis-implications-for-acute-kidney-injury
#17
Carla S Ceron, Celine Baligand, Sunil Joshi, Shaynah Wanga, Patrick M Cowley, Joy P Walker, Sang Heon Song, Rajeev Mahimkar, Anthony J Baker, Robert L Raffai, Zhen J Wang, David H Lovett
Acute kidney injury (AKI) causes severe morbidity, mortality, and chronic kidney disease (CKD). Mortality is particularly marked in the elderly and with preexisting CKD. Oxidative stress is a common theme in models of AKI induced by ischemia-reperfusion (I-R) injury. We recently characterized an intracellular isoform of matrix metalloproteinase-2 (MMP-2) induced by oxidative stress-mediated activation of an alternate promoter in the first intron of the MMP-2 gene. This generates an NH2-terminal truncated MMP-2 (NTT-MMP-2) isoform that is intracellular and associated with mitochondria...
June 1, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28329914/ginsenoside-rg3-restores-hepatitis-c-virus-induced-aberrant-mitochondrial-dynamics-and-inhibits-virus-propagation
#18
Seong-Jun Kim, Jae Young Jang, Eun-Jung Kim, Eun Kyung Cho, Dae-Gyun Ahn, Chonsaeng Kim, Han Seul Park, Soung Won Jeong, Sae Hwan Lee, Sang Gyune Kim, Young Seok Kim, Hong Soo Kim, Boo Sung Kim, Jihyung Lee, Aleem Siddiqui
Hepatitis C virus (HCV) alters mitochondrial dynamics associated with persistent viral infection and suppression of innate immunity. Mitochondrial dysfunction is also a pathologic feature of direct-acting antiviral (DAA) treatment. Despite the high efficacy of DAAs, their use in treating patients with chronic hepatitis C in interferon-sparing regimens occasionally produces undesirable side effects such as fatigue, migraine, and other conditions, which may be linked to mitochondrial dysfunction. Here, we show that clinically prescribed DAAs, including sofosbuvir, affect mitochondrial dynamics...
September 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28271436/the-tbk1-optn-axis-mediates-crosstalk-between-mitophagy-and-the-innate-immune-response-a-potential-therapeutic-target-for-neurodegenerative-diseases
#19
Lu He, Linxi Chen, Lanfang Li
No abstract text is available yet for this article.
June 2017: Neuroscience Bulletin
https://www.readbyqxmd.com/read/28148298/tbk1-a-new-player-in-als-linking-autophagy-and-neuroinflammation
#20
REVIEW
James A Oakes, Maria C Davies, Mark O Collins
Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disorder affecting motor neurons, resulting in progressive muscle weakness and death by respiratory failure. Protein and RNA aggregates are a hallmark of ALS pathology and are thought to contribute to ALS by impairing axonal transport. Mutations in several genes known to contribute to ALS result in deposition of their protein products as aggregates; these include TARDBP, C9ORF72, and SOD1. In motor neurons, this can disrupt transport of mitochondria to areas of metabolic need, resulting in damage to cells and can elicit a neuroinflammatory response leading to further neuronal damage...
February 2, 2017: Molecular Brain
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