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https://www.readbyqxmd.com/read/29050006/recent-insights-into-the-biological-functions-of-sestrins-in-health-and-disease
#1
Menglong Wang, Yao Xu, Jianfang Liu, Jing Ye, Wenhui Yuan, Huimin Jiang, Zhen Wang, Hong Jiang, Jun Wan
Sestrins (Sesns) have been identified as a family of highly conserved stress-inducible proteins that are strongly up-regulated by various stresses, including DNA damage, oxidative stress, and hypoxia. The Sesns play protective roles in most physiological and pathological conditions mainly through the regulation of oxidative stress, inflammation, autophagy, endoplasmic reticulum stress, and metabolic homeostasis. In this review, we discussed the possible regulators of Sesns expression, such as p53, forkhead box O, nuclear factor erythroid 2 like 2 (Nrf2), NH (2)-terminal kinase (JNK)/c-Jun pathway and hypoxia-inducible factor-1α (Hif-1α), and the downstream pathways regulated by the Sesns including AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling, mitogen-activated protein kinases (MAPKs) signaling, Nrf2 signaling, NADPH oxidase signaling and transforming growth factor β (TGF-β) signaling in heart diseases, lung diseases, gastrointestinal tract diseases, liver and metabolism diseases, neurological diseases, kidney diseases and immunological diseases...
October 19, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29047102/reactive-oxygen-species-in-copd-related-vascular-remodeling
#2
Li Zuo, Chia-Chen Chuang, Alexander D Clark, Davis E Garrison, Jamie L Kuhlman, David C Sypert
The pathogenesis of chronic obstructive pulmonary disease (COPD) is a multifaceted process involving the alteration of pulmonary vasculature. Such vascular remodeling can be associated with inflammation, shear stress, and hypoxia-conditions commonly seen in patients with lung diseases. Particularly, the overproduction of reactive oxygen species (ROS) in the diseased lungs contributes greatly to pulmonary vascular remodeling. ROS play an important role in vascular homeostasis, yet excessive ROS can alter pulmonary vasculature and impair lung function, as implicated in COPD at all stages...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047086/natural-antioxidants-as-potential-therapy-and-a-promising-role-for-melatonin-against-pulmonary-hypertension
#3
Gerald J Maarman
Plasma and serum samples, and lung/heart tissue of pulmonary hypertension (PH) patients and animal models of PH display elevated oxidative stress. Moreover, the severity of PH and levels of oxidative stress increase concurrently, which suggests that oxidative stress could be utilized as a biomarker for PH progression. Accumulating evidence has well established that oxidative stress is also key role player in the development of PH. Preclinical studies have demonstrated that natural antioxidants improved PH condition, and, therefore, antioxidant therapy has been proposed as a potential therapeutic strategy against PH...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047085/redox-dependent-calpain-signaling-in-airway-and-pulmonary-vascular-remodeling-in-copd
#4
Laszlo Kovacs, Yunchao Su
The calcium-dependent cytosolic, neutral, thiol endopeptidases, calpains, perform limited cleavage of their substrates thereby irreversibly changing their functions. Calpains have been shown to be involved in several physiological processes such as cell motility, proliferation, cell cycle, signal transduction, and apoptosis. Overactivation of calpain or mutations in the calpain genes contribute to a number of pathological conditions including neurodegenerative disorders, rheumatoid arthritis, cancer, and lung diseases...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047084/ros-signaling-in-the-pathogenesis-of-acute-lung-injury-ali-and-acute-respiratory-distress-syndrome-ards
#5
Manuela Kellner, Satish Noonepalle, Qing Lu, Anup Srivastava, Evgeny Zemskov, Stephen M Black
The generation of reactive oxygen species (ROS) plays an important role for the maintenance of cellular processes and functions in the body. However, the excessive generation of oxygen radicals under pathological conditions such as acute lung injury (ALI) and its most severe form acute respiratory distress syndrome (ARDS) leads to increased endothelial permeability. Within this hallmark of ALI and ARDS, vascular microvessels lose their junctional integrity and show increased myosin contractions that promote the migration of polymorphonuclear leukocytes (PMNs) and the transition of solutes and fluids in the alveolar lumen...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047079/molecular-basis-of-nitrative-stress-in-the-pathogenesis-of-pulmonary-hypertension
#6
Colin E Evans, You-Yang Zhao
Pulmonary hypertension (PH) is a lung vascular disease with marked increases in pulmonary vascular resistance and pulmonary artery pressure (>25 mmHg at rest). In PH patients, increases in pulmonary vascular resistance lead to impaired cardiac output and reduced exercise tolerance. If untreated, PH progresses to right heart failure and premature lethality. The mechanisms that control the pathogenesis of PH are incompletely understood, but evidence from human and animal studies implicate nitrative stress in the development of PH...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047037/diesel-exhaust-particles-and-the-induction-of-macrophage-activation-and-dysfunction
#7
REVIEW
Akeem O Lawal
Diesel exhaust particles (DEP) are an important component of air particulate matter, generated from the incomplete combustion of fossil fuel in diesel engines. Several epidemiological and experimental data have shown the ability of DEP to induce oxidative stress and pro-inflammatory response as mechanisms in macrophage activation and dysfunction. Macrophages are very important to immunity and immune response due to their ability to phagocyte microbes and parasites. They also respond to toxic chemicals, such as DEP, in the environment and studies have shown that their functions may be impaired by their exposure to DEP...
October 19, 2017: Inflammation
https://www.readbyqxmd.com/read/29046030/-immunopathology-of-chronic-obstructive-pulmonary-disease
#8
Nora Ernestina Martínez-Aguilar, María Eugenia Vargas-Camaño, Rogelio Ramsés Hernández-Pliego, Genny Margarita Chaia-Semerena, María Rosario Pérez-Chavira
Chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable condition that has a complex pathophysiology and an even more complex immunopathological process. The purpose of this review was to analyze COPD immunopathological aspects, which was addressed by undertaking a literature search for the most relevant documents indexed in the PubMed database over the last 10 years. Different conclusions could be drawn: in COPD immunopathology there are immune and non-immune inflammatory changes with oxidative stress imbalance, there are alterations in the protease/anti-protease ratio caused by direct and indirect genetic and epigenetic-environmental defects; COPD produces irreversible tissue damage and chronic inflammation with tissue repair alteration, which induces chronic obstruction of the airway, bronchitis and systemic damage...
July 2017: Revista Alergia Mexico: Organo Oficial de la Sociedad Mexicana de Alergia e Inmunología, A.C
https://www.readbyqxmd.com/read/29045843/high-throughput-functional-genetic-and-compound-screens-identify-targets-for-senescence-induction-in-cancer
#9
Liqin Wang, Rodrigo Leite de Oliveira, Cun Wang, João M Fernandes Neto, Sara Mainardi, Bastiaan Evers, Cor Lieftink, Ben Morris, Fleur Jochems, Lisa Willemsen, Roderick L Beijersbergen, René Bernards
Senescence is a proliferation arrest that can result from a variety of stresses. Cancer cells can also undergo senescence, but the stresses that provoke cancer cells to undergo senescence are unclear. Here, we use both functional genetic and compound screens in cancer cells harboring a reporter that is activated during senescence to find targets that induce senescence. We show that suppression of the SWI/SNF component SMARCB1 induces senescence in melanoma through strong activation of the MAP kinase pathway...
October 17, 2017: Cell Reports
https://www.readbyqxmd.com/read/29043785/elevated-exposures-to-polycyclic-aromatic-hydrocarbons-and-other-organic-mutagens-in-ottawa-firefighters-participating-in-emergency-on-shift-fire-suppression
#10
Jennifer L A Keir, Umme S Akhtar, David M J Matschke, Tracy L Kirkham, Hing Man Chan, Pierre Ayotte, Paul A White, Jules M Blais
Occupational exposures to combustion emissions were examined in Ottawa Fire Service (OFS) firefighters. Paired urine and dermal wipe samples (i.e., pre- and post-event) as well as personal air samples and fire event questionnaires were collected from 27 male OFS firefighters. A total of 18 OFS office workers were used as additional controls. Exposures to polycyclic aromatic hydrocarbons (PAHs) and other organic mutagens were assessed by quantification of urinary PAH metabolite levels, levels of PAHs in dermal wipes and personal air samples, and urinary mutagenicity using the Salmonella mutagenicity assay (Ames test)...
October 18, 2017: Environmental Science & Technology
https://www.readbyqxmd.com/read/29042934/intermittent-hypoxia-simulating-obstructive-sleep-apnea-causes-pulmonary-inflammation-and-activates-the-nrf2-ho-1-pathway
#11
Yeying Wang, Yanling Chai, Xiaojie He, Li Ai, Xia Sun, Yiling Huang, Yongxia Li
Obstructive sleep apnea (OSA) is a disorder with high morbidity in adults. OSA damages multiple organs and tissues, including the cardiovascular and cerebrovascular systems, the metabolism system, the lungs, liver and heart. OSA-induced damage is earliest and greatest to the pulmonary tissue. The present study established a rat OSA model of differing severity by inducing intermittent hypoxia with different concentrations of O2 and it was determined that OSA caused a severe oxidative stress response and pulmonary inflammation in a dose-dependent manner...
October 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29042481/the-matricellular-protein-tsp1-promotes-human-and-mouse-endothelial-cell-senescence-through-cd47-and-nox1
#12
Daniel N Meijles, Sanghamitra Sahoo, Imad Al Ghouleh, Jefferson H Amaral, Raquel Bienes-Martinez, Heather E Knupp, Shireen Attaran, John C Sembrat, Seyed M Nouraie, Mauricio M Rojas, Enrico M Novelli, Mark T Gladwin, Jeffrey S Isenberg, Eugenia Cifuentes-Pagano, Patrick J Pagano
Senescent cells withdraw from the cell cycle and do not proliferate. The prevalence of senescent compared to normally functioning parenchymal cells increases with age, impairing tissue and organ homeostasis. A contentious principle governing this process has been the redox theory of aging. We linked matricellular protein thrombospondin 1 (TSP1) and its receptor CD47 to the activation of NADPH oxidase 1 (Nox1), but not of the other closely related Nox isoforms, and associated oxidative stress, and to senescence in human cells and aged tissue...
October 17, 2017: Science Signaling
https://www.readbyqxmd.com/read/29040326/mycobacterium-tuberculosis-infection-modulates-adipose-tissue-biology
#13
Macarena Beigier-Bompadre, Georgina N Montagna, Anja A Kühl, Laura Lozza, January Weiner, Andreas Kupz, Alexis Vogelzang, Hans-Joachim Mollenkopf, Delia Löwe, Silke Bandermann, Anca Dorhoi, Volker Brinkmann, Kai Matuschewski, Stefan H E Kaufmann
Mycobacterium tuberculosis (Mtb) primarily resides in the lung but can also persist in extrapulmonary sites. Macrophages are considered the prime cellular habitat in all tissues. Here we demonstrate that Mtb resides inside adipocytes of fat tissue where it expresses stress-related genes. Moreover, perigonadal fat of Mtb-infected mice disseminated the infection when transferred to uninfected animals. Adipose tissue harbors leukocytes in addition to adipocytes and other cell types and we observed that Mtb infection induces changes in adipose tissue biology depending on stage of infection...
October 17, 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/29039230/effect-of-prenatal-waterpipe-tobacco-smoke-on-airway-inflammation-in-murine-model-of-asthma-of-adult-offspring-mice
#14
Nour A Al-Sawalha, Hanadi F Al-Bo'ul, Karem H Alzoubi, Omar F Khabour, Vaidehi J Thanawala
OBJECTIVE: Worldwide popularity of waterpipe tobacco smoking has increased, including in pregnant women. This study investigates the effect of prenatal waterpipe tobacco smoke (WTS) exposure on airway inflammation in a murine model of asthma of adult offspring mice. MATERIALS AND METHODS: Pregnant BALB/c mice were exposed to fresh air or WTS, using a whole-body exposure system that mimics human use during WTS. Adult male offspring mice were divided into; (1) control (prenatal fresh air, postnatal ovalbumin sensitization and saline challenge), (2) postnatal Ova S/C (prenatal fresh air, postnatal ovalbumin sensitization and challenge (Ova S/C)), (3) prenatal WTS (prenatal WTS, postnatal ovalbumin sensitization and saline challenge) and (4) prenatal WTS + postnatal Ova S/C...
July 2017: Inhalation Toxicology
https://www.readbyqxmd.com/read/29039225/toxicological-impact-of-waterpipe-smoking-and-flavorings-in-the-oral-cavity-and-respiratory-system
#15
Fawad Javed, Shatha Subhi ALHarthi, Munerah Saleh BinShabaib, Sangeeta Gajendra, Georgios E Romanos, Irfan Rahman
Waterpipe smoking (WS), an emerging trend has major health concerns. It is prevalent worldwide as a recreational activity both indoors and outdoors. The aim of this review was to assess the impact of waterpipe smoke on the oral and respiratory system (oral cavity and pulmonary tissues). A number of studies have shown that periodontal health status is compromised in waterpipe smokers when compared with nonsmokers. Some studies have associated WS with oral premalignant and malignant lesions; however, due to the poor quality of these studies, the presented outcomes should be interpreted with caution...
October 17, 2017: Inhalation Toxicology
https://www.readbyqxmd.com/read/29038367/a-nonimmune-function-of-t-cells-in-promoting-lung-tumor-progression
#16
Jesse A Green, Nicholas Arpaia, Michail Schizas, Anton Dobrin, Alexander Y Rudensky
The involvement of effector T cells and regulatory T (T reg) cells in opposing and promoting solid organ carcinogenesis, respectively, is viewed as a shifting balance between a breach versus establishment of tolerance to tumor or self-antigens. We considered that tumor-associated T cells might promote malignancy via distinct mechanisms used by T cells in nonlymphoid organs to assist in their maintenance upon injury or stress. Recent studies suggest that T reg cells can participate in tissue repair in a manner separable from their immunosuppressive capacity...
October 16, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29038055/serum-and-brain-purine-levels-in-an-experimental-systemic-infection-of-mice-by-cryptococcus-neoformans-purinergic-immunomodulatory-effects
#17
Maria Isabel de Azevedo, Aleksandro S Da Silva, Laerte Ferreiro, Pedro H Doleski, Alexandre A Tonin, Emerson A Casali, Cesar E J Moritz, Gabriel H Schirmbeck, Valesca V Cardoso, Mariana M Flores, Rafael Fighera, Janio M Santurio
The aim of this study was to evaluate the purine levels in serum and brains of mice experimentally infected by Cryptococcus neoformans. Twenty-four mice were divided into the following groups: a control group (n = 12; Group A) and an infection group with animals that were infected (n = 12; Group B) with a 0.3-mL intraperitoneal injection containing 1.7 × 10(7)C. neoformans cells. Blood and brains were collected on days 20 (n = 6 per group) and 50 (n = 6 per group) post-infection (PI). Histopathology and lung and brain cultures were performed to confirm fungal infection and tissue injuries...
October 13, 2017: Microbial Pathogenesis
https://www.readbyqxmd.com/read/29033840/hydrogen-sulfide-inhibits-cigarette-smoke-induced-endoplasmic-reticulum-stress-and-apoptosis-in-bronchial-epithelial-cells
#18
Fan Lin, Chengcheng Liao, Yun Sun, Jinsheng Zhang, Weiwei Lu, Yu Bai, Yixuan Liao, Minxia Li, Xianqiang Ni, Yuelong Hou, Yongfen Qi, Yahong Chen
Background: Apoptosis of lung structural cells contributes to the process of lung damage and remodeling in chronic obstructive pulmonary disease (COPD). Our previous studies demonstrated that exogenous hydrogen sulfide (H2S) can reduce the lung tissue pathology score, anti-inflammation and anti-oxidation effects in COPD, but the effect of H2S in regulating cigarette smoke (CS) induced bronchial epithelial cell apoptosis and the underlying mechanisms are not clear. Objectives: To investigate the effect of H2S on CS induced endoplasmic reticulum stress (ERS) and bronchial epithelial cell apoptosis...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29032072/oxidative-stress-prediction-a-preliminary-approach-using-a-response-surface-based-technique
#19
M Sierra, L Bragg-Gonzalo, J Grasa, M J Muñoz, D González, F J Miana-Mena
A response surface was built to predict the lipid peroxidation level, generated in an iron-ascorbate in vitro model, of any organ, which is correlated with the oxidative stress injury in biological membranes. Oxidative stress studies are numerous, usually performed on laboratory animals. However, ethical concerns require validated methods to reduce the use of laboratory animals. The response surface described here is a validated method to replace animals. Tissue samples of rabbit liver, kidney, heart, skeletal muscle and brain were oxidized with different concentrations of FeCl3 (0...
October 12, 2017: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/29029603/the-pathophysiological-role-of-mitochondrial-oxidative-stress-in-lung-diseases
#20
REVIEW
Xiaojing Liu, Zhihong Chen
Mitochondria are critically involved in reactive oxygen species (ROS)-dependent lung diseases, such as lung fibrosis, asbestos, chronic airway diseases and lung cancer. Mitochondrial DNA (mtDNA) encodes mitochondrial proteins and is more sensitive to oxidants than nuclear DNA. Damage to mtDNA causes mitochondrial dysfunction, including electron transport chain impairment and mitochondrial membrane potential loss. Furthermore, damaged mtDNA also acts as a damage-associated molecular pattern (DAMP) that drives inflammatory and immune responses...
October 13, 2017: Journal of Translational Medicine
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