keyword
MENU ▼
Read by QxMD icon Read
search

mitophagy immune

keyword
https://www.readbyqxmd.com/read/28366813/mita-modulated-autophagy-flux-promotes-cell-death-in-breast-cancer-cells
#1
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
#2
Carla S Ceron, Celine Baligand, Sunil K 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 pre-existing 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 N-terminal truncated MMP-2 isoform (NTT-MMP-2) that is intracellular and associated with mitochondria...
March 22, 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
#3
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, Ji-Hyung 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 treatment of 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...
March 22, 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
#4
Lu He, Linxi Chen, Lanfang Li
No abstract text is available yet for this article.
March 7, 2017: Neuroscience Bulletin
https://www.readbyqxmd.com/read/28148298/tbk1-a-new-player-in-als-linking-autophagy-and-neuroinflammation
#5
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
https://www.readbyqxmd.com/read/28026986/xenophagy-a-battlefield-between-host-and-microbe-and-a-possible-avenue-for-cancer-treatment
#6
Kai Mao, Daniel J Klionsky
In eukaryotes, xenophagy is defined as a type of selective macroautophagy/autophagy that is used for eliminating invading pathogens. In contrast to other types of selective autophagy, such as mitophagy, pexophagy and ribophagy, xenophagy is used by eukaryotes for targeting microbes-hence the prefix "xeno" meaning "other" or "foreign"-that have infected a host cell, leading to their lysosomal degradation. This unique characteristic links xenophagy to antibacterial and antiviral defenses, as well as the immune response...
February 2017: Autophagy
https://www.readbyqxmd.com/read/27881606/mitochondria-protection-after-acute-ischemia-prevents-prolonged-upregulation-of-il-1%C3%AE-and-il-18-and-arrests-ckd
#7
Hazel H Szeto, Shaoyi Liu, Yi Soong, Surya V Seshan, Leona Cohen-Gould, Viacheslav Manichev, Leonard C Feldman, Torgny Gustafsson
The innate immune system has been implicated in both AKI and CKD. Damaged mitochondria release danger molecules, such as reactive oxygen species, DNA, and cardiolipin, which can cause NLRP3 inflammasome activation and upregulation of IL-18 and IL-1β It is not known if mitochondrial damage persists long after ischemia to sustain chronic inflammasome activation. We conducted a 9-month study in Sprague-Dawley rats after 45 minutes of bilateral renal ischemia. We detected glomerular and peritubular capillary rarefaction, macrophage infiltration, and fibrosis at 1 month...
November 23, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27867381/a-critical-reappraisal-of-neutrophil-extracellular-traps-and-netosis-mimics-based-on-differential-requirements-for-protein-citrullination
#8
Maximilian F Konig, Felipe Andrade
NETosis, an antimicrobial form of neutrophil cell death, is considered a primary source of citrullinated autoantigens in rheumatoid arthritis (RA) and immunogenic DNA in systemic lupus erythematosus (SLE). Activation of the citrullinating enzyme peptidylarginine deiminase type 4 (PAD4) is believed to be essential for neutrophil extracellular trap (NET) formation and NETosis. PAD4 is therefore viewed as a promising therapeutic target to inhibit the formation of NETs in both diseases. In this review, we examine the evidence for PAD4 activation during NETosis and provide experimental data to suggest that protein citrullination is not a universal feature of NETs...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/27789101/inflammaging-and-garb-aging
#9
REVIEW
Claudio Franceschi, Paolo Garagnani, Giovanni Vitale, Miriam Capri, Stefano Salvioli
'Inflammaging' refers to the chronic, low-grade inflammation that characterizes aging. Inflammaging is macrophage centered, involves several tissues and organs, including the gut microbiota, and is characterized by a complex balance between pro- and anti-inflammatory responses. Based on literature data, we argue that the major source of inflammatory stimuli is represented by endogenous/self, misplaced, or altered molecules resulting from damaged and/or dead cells and organelles (cell debris), recognized by receptors of the innate immune system...
March 2017: Trends in Endocrinology and Metabolism: TEM
https://www.readbyqxmd.com/read/27636016/mesenchymal-stromal-cells-deficient-in-autophagy-proteins-are-susceptible-to-oxidative-injury-and-mitochondrial-dysfunction
#10
Sailaja Ghanta, Konstantin Tsoyi, Xiaoli Liu, Kiichi Nakahira, Bonna Ith, Anna A Coronata, Laura E Fredenburgh, Joshua A Englert, Claude A Piantadosi, Augustine M K Choi, Mark A Perrella
Oxidative stress resulting from inflammatory responses that occur during acute lung injury and sepsis can initiate changes in mitochondrial function. Autophagy regulates cellular processes in the setting of acute lung injury, sepsis, and oxidative stress by modulating the immune response and facilitating turnover of damaged cellular components. We have shown that mesenchymal stromal cells (MSCs) improve survival in murine models of sepsis by also regulating the immune response. However, the effect of autophagy on MSCs and MSC mitochondrial function during oxidative stress is unknown...
March 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/27629285/autophagy-inhibition-and-mitochondrial-remodeling-join-forces-to-amplify-apoptosis-in-activation-induced-cell-death
#11
Corrado Mauro, Campello Silvia
Mitochondrial structural and functional changes and the autophagy pathway crosstalk under several stress conditions. However, their interplay under physiological cell death stimulation has been unclear. In our recent report, we show that during activation-induced cell death (AICD), the T-cell receptor (TCR)-dependent pathway that controls immune tolerance, autophagy is inhibited at an early stage. Further, we found that this inhibition is coupled with mitochondria fragmentation and cristae remodeling to unleash the apoptotic program...
December 2016: Autophagy
https://www.readbyqxmd.com/read/27558401/is-cancer-a-severe-delayed-hypersensitivity-reaction-and-histamine-a-blueprint
#12
Mahin Khatami
Longevity and accumulation of multiple context-dependent signaling pathways of long-standing inflammation (antigen-load or oxidative stress) are the results of decreased/altered regulation of immunity and loss of control switch mechanisms that we defined as Yin and Yang of acute inflammation or immune surveillance. Chronic inflammation is initiated by immune disruptors-induced progressive changes in physiology and function of susceptible host tissues that lead to increased immune suppression and multistep disease processes including carcinogenesis...
December 2016: Clinical and Translational Medicine
https://www.readbyqxmd.com/read/27496003/exposure-to-zidovudine-adversely-affects-mitochondrial-turnover-in-primary-t-cells
#13
Zoë R Wallace, Sharon Sanderson, Anna Katarina Simon, Lucy Dorrell
Zidovudine (ZDV) is a widely used component of antiretroviral therapy (ART) in resource-limited settings, despite its known adverse effects, which include mitochondrial toxicity in muscle, liver and adipose tissue. It has also been associated with impaired immunological recovery. We hypothesised that ZDV might impair mitochondrial health and survival of primary T cells. We performed a cross-sectional analysis of mitochondrial function, mitophagy and susceptibility to apoptosis in healthy donor primary T cells after exposure to ZDV in vitro, together with T cells from patients who were virologically suppressed on ZDV-containing ART regimens for ≥1 year and age-matched subjects receiving non-ZDV ART regimens...
September 2016: Antiviral Research
https://www.readbyqxmd.com/read/27458013/mycotoxin-patulin-suppresses-innate-immune-responses-by-mitochondrial-dysfunction-and-p62-sequestosome-1-dependent-mitophagy
#14
Wan-Ting Tsai, Yin-Chiu Lo, Ming-Sian Wu, Chia-Yang Li, Yi-Ping Kuo, Yi-Hui Lai, Yu Tsai, Kai-Chieh Chen, Tsung-Hsien Chuang, Chun-Hsu Yao, Jinq-Chyi Lee, Li-Chung Hsu, John T-A Hsu, Guann-Yi Yu
Innate immune responses are important for pathogen elimination and adaptive immune response activation. However, excess inflammation may contribute to immunopathology and disease progression (e.g. inflammation-associated hepatocellular carcinoma). Immune modulation resulting from pattern recognition receptor-induced responses is a potential strategy for controlling immunopathology and related diseases. This study demonstrates that the mycotoxin patulin suppresses Toll-like receptor- and RIG-I/MAVS-dependent cytokine production through GSH depletion, mitochondrial dysfunction, the activation of p62-associated mitophagy, and p62-TRAF6 interaction...
September 9, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27439607/mitophagy-a-balance-regulator-of-nlrp3-inflammasome-activation
#15
REVIEW
Min-Ji Kim, Joo-Heon Yoon, Ji-Hwan Ryu
The NLRP3 inflammasome is activated by a variety of external or host-derived stimuli and its activation initiates an inflammatory response through caspase-1 activation, resulting in inflammatory cytokine IL-1β maturation and secretion. The NLRP3 inflammasome activation is a kind of innate immune response, most likely mediated by myeloid cells acting as a host defense mechanism. However, if this activation is not properly regulated, excessive inflammation induced by overactivated NLRP3 inflammasome can be detrimental to the host, causing tissue damage and organ dysfunction, eventually causing several diseases...
October 2016: BMB Reports
https://www.readbyqxmd.com/read/27390127/macroautophagy-inhibition-maintains-fragmented-mitochondria-to-foster-t-cell-receptor-dependent-apoptosis
#16
Mauro Corrado, Francesca R Mariotti, Laura Trapani, Lucia Taraborrelli, Francesca Nazio, Valentina Cianfanelli, Maria Eugenia Soriano, Emilie Schrepfer, Francesco Cecconi, Luca Scorrano, Silvia Campello
Mitochondrial dynamics and functionality are linked to the autophagic degradative pathway under several stress conditions. However, the interplay between mitochondria and autophagy upon cell death signalling remains unclear. The T-cell receptor pathway signals the so-called activation-induced cell death (AICD) essential for immune tolerance regulation. Here, we show that this apoptotic pathway requires the inhibition of macroautophagy. Protein kinase-A activation downstream of T-cell receptor signalling inhibits macroautophagy upon AICD induction...
August 15, 2016: EMBO Journal
https://www.readbyqxmd.com/read/27347716/iron-depletion-promotes-mitophagy-to-maintain-mitochondrial-integrity-in-pathogenic-yeast-candida-glabrata
#17
Minoru Nagi, Koichi Tanabe, Hironobu Nakayama, Keigo Ueno, Satoshi Yamagoe, Takashi Umeyama, Hideaki Ohno, Yoshitsugu Miyazaki
Candida glabrata, a haploid budding yeast, is the cause of severe systemic infections in immune-compromised hosts. The amount of free iron supplied to C. glabrata cells during systemic infections is severely limited by iron-chelating proteins such as transferrin. Thus, the iron-deficiency response in C. glabrata cells is thought to play important roles in their survival inside the host's body. In this study, we found that mitophagy was induced under iron-depleted conditions, and that the disruption of a gene homologous to ATG32, which is responsible for mitophagy in Saccharomyces cerevisiae, blocked mitophagy in C...
August 2, 2016: Autophagy
https://www.readbyqxmd.com/read/27345367/parkinson-s-disease-related-proteins-pink1-and-parkin-repress-mitochondrial-antigen-presentation
#18
Diana Matheoud, Ayumu Sugiura, Angélique Bellemare-Pelletier, Annie Laplante, Christiane Rondeau, Magali Chemali, Ali Fazel, John J Bergeron, Louis-Eric Trudeau, Yan Burelle, Etienne Gagnon, Heidi M McBride, Michel Desjardins
Antigen presentation is essential for establishing immune tolerance and for immune responses against infectious disease and cancer. Although antigen presentation can be mediated by autophagy, here we demonstrate a pathway for mitochondrial antigen presentation (MitAP) that relies on the generation and trafficking of mitochondrial-derived vesicles (MDVs) rather than on autophagy/mitophagy. We find that PINK1 and Parkin, two mitochondrial proteins linked to Parkinson's disease (PD), actively inhibit MDV formation and MitAP...
July 14, 2016: Cell
https://www.readbyqxmd.com/read/27133164/fanconi-anemia-proteins-function-in-mitophagy-and-immunity
#19
Rhea Sumpter, Shyam Sirasanagandla, Álvaro F Fernández, Yongjie Wei, Xiaonan Dong, Luis Franco, Zhongju Zou, Christophe Marchal, Ming Yeh Lee, D Wade Clapp, Helmut Hanenberg, Beth Levine
Fanconi anemia (FA) pathway genes are important tumor suppressors whose best-characterized function is repair of damaged nuclear DNA. Here, we describe an essential role for FA genes in two forms of selective autophagy. Genetic deletion of Fancc blocks the autophagic clearance of viruses (virophagy) and increases susceptibility to lethal viral encephalitis. Fanconi anemia complementation group C (FANCC) protein interacts with Parkin, is required in vitro and in vivo for clearance of damaged mitochondria, and decreases mitochondrial reactive oxygen species (ROS) production and inflammasome activation...
May 5, 2016: Cell
https://www.readbyqxmd.com/read/27093228/biology-and-metabolism-of-sepsis-innate-immunity-bioenergetics-and-autophagy
#20
REVIEW
Anthony J Lewis, Timothy R Billiar, Matthew R Rosengart
Sepsis is a complex, heterogeneous physiologic condition that represents a significant public health concern. While many insights into the pathophysiology of sepsis have been elucidated over the past decades of research, important questions remain. This article serves as a review of several important areas in sepsis research. Understanding the innate immune response has been at the forefront as of late, especially in the context of cytokine-directed therapeutic trials. Cellular bioenergetic changes provide insight into the development of organ dysfunction in sepsis...
June 2016: Surgical Infections
keyword
keyword
87910
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"