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Antioxidants & Redox Signaling

David Fulton, Xueyi Li, Zsuzsanna Bordan, Yusi Wang, Keyvan Mahboubi, Radu Daniel Rudic, Stephen Haigh, Feng Chen, Scott A Barman
SIGNIFICANCE: Pulmonary Arterial Hypertension (PAH) is a progressive disease arising from the narrowing of pulmonary arteries (PA) resulting in high pulmonary arterial blood pressure and ultimately right ventricular (RV) failure. A defining characteristic of PAH is the excessive and unrelenting inward remodeling of PA that includes increased proliferation, inflammation and fibrosis. CRITICAL ISSUES: There is no cure for PAH nor interventions that effectively arrest or reverse PA remodeling and intensive research over the past several decades has sought to identify novel molecular mechanisms of therapeutic value...
February 15, 2019: Antioxidants & Redox Signaling
Ruslan Rafikov, Vineet Nair, Shripad Sinari, Harini Babu, Jennifer C Sullivan, Jason X-J Yuan, Ankit A Desai, Olga Rafikova
AIMS: Pulmonary arterial hypertension (PAH) is a progressive lethal disease with a known gender dimorphism. While females are more susceptible to PAH, male patients have a lower survival rate. Initial pulmonary vascular damage plays an important role in PAH pathogenesis. Therefore, this study aimed to investigate the role of gender in activation of apoptosis/necrosis mediated signaling pathways in PAH. RESULTS: The media collected from pulmonary artery endothelial cells (PAECs) died by necrosis or apoptosis was used to treat naïve PAECs...
January 17, 2019: Antioxidants & Redox Signaling
Ting Gong, Ann C Hashimoto, Alexandru R Sasuclark, Vedbar S Khadka, Alexandra Gurary, Matthew W Pitts
AIMS: Selenoproteins are an essential class of proteins involved in redox signaling and energy metabolism. However, the functions of many selenoproteins are not clearly established. Selenoprotein M (SELENOM), an ER-resident oxidoreductase bearing structural similarity to thioredoxin (TXN), is among those yet to be fully characterized. This protein is highly expressed in hypothalamic regions involved in leptin signaling and has been previously linked to energy metabolism. Herein, we performed a series of studies using in vivo and in vitro models to probe the specific influence of SELENOM on hypothalamic leptin signaling and assess SELENOM-regulated pathways...
January 16, 2019: Antioxidants & Redox Signaling
Gaston Ofman, Trent E Tipple
SIGNIFICANCE: Redox homeostasis is finely tuned and governed by distinct intracellular mechanisms. The dysregulation of this either by external or internal events is a fundamental pathophysiologic base for many pulmonary diseases. Recent Advances: Based on recent discoveries, it is increasingly clear that cellular redox state and oxidation of signaling molecules are critical modulators of lung disease and represent a final common pathway that leads to poor respiratory outcomes. CRITICAL ISSUES: Based on the wide variety of stimuli that alter specific redox signaling pathways, improved understanding of the disease and patient-specific alterations is needed for the developing of therapeutic targets...
January 16, 2019: Antioxidants & Redox Signaling
Evgeny Zemskov, Qing Lu, Wojciech Wojciech Ornatowski, Christina N Klinger, Ankit A Desai, Emin Maltepe, Jason X-J Yuan, Ting Wang, Jeffrey R Fineman, Stephen Black
As our fundamental understanding of the underlying causes of lung disease has increased it has become evident that oxidative stress plays a critical role. Oxidative stress in the cell is characterized by excessive generation of reactive oxygen species (ROS). Superoxide (O2-) and hydrogen peroxide (H2O2) are the main ROS involved in the regulation of cellular metabolism. A number of cells in the lung both produce, and respond to, ROS. These include vascular endothelial- (ECs) and smooth muscle (SMCs) cells, fibroblasts, and epithelial cells as well as the cells involved in the inflammatory response, including macrophages, neutrophils, eosinophils...
January 9, 2019: Antioxidants & Redox Signaling
Sergey I Dikalov, Anna Dikalova
SIGNIFICANCE: Vascular dysfunction plays a key role in the development of arteriosclerosis, heart disease and hypertension which causes one-third of deaths worldwide. Vascular oxidative stress and metabolic disorders contribute to vascular dysfunction leading to impaired vasorelaxation, vascular hypertrophy, fibrosis and aortic stiffening. Mitochondria are critical in the regulation of metabolic and antioxidant functions; therefore, mitochondria targeted treatments could be beneficial...
January 8, 2019: Antioxidants & Redox Signaling
Daniel Winnica, Catherine Corey, Steven Mullett, Michael Reynolds, Gabrielle Hill, Stacy Wendell, Loretta Que, Fernando Holguin, Sruti Shiva
AIMS: Asthma, characterized by airway obstruction and hyper-responsiveness, is more severe and less responsive to treatment in obese subjects. While alterations in mitochondrial function and redox signaling have been implicated in pathogenesis, it is unclear whether these mechanisms differ in lean versus obese asthmatics. Additionally, we previously demonstrated that circulating platelets from asthmatics individuals have altered bioenergetics; however, it is unknown whether platelet mitochondrial changes reflect those observed in airway epithelial cells...
January 4, 2019: Antioxidants & Redox Signaling
Hagir Badawi Suliman, Eva Nozik-Grayck
Pulmonary hypertension (PH) is a progressive disease characterized by pulmonary vascular remodeling and lung vasculopathy. The disease displays progressive dyspnea, pulmonary artery uncoupling, and right ventricular (RV) dysfunction. The molecular events that promote the development of pulmonary hypertension are complex and incompletely understood. Metabolic impairment has been proposed to contribute to the pathophysiology of PH with evidence for mitochondrial dysfunction involving the electron transport chain proteins, antioxidant enzymes, apoptosis regulators and mitochondrial quality control...
January 3, 2019: Antioxidants & Redox Signaling
Valerio Nobili, Anna Alisi, Antonella Mosca, Annalisa Crudele, Salvatore Zaffina, Marcella Denaro, Antonella Smeriglio, Domenico Trombetta
TRIAL DESIGN: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in children. Several studies suggest that the improvement of oxidative stress is suggested as a possible therapeutic strategy for paediatric NASH. We performed a randomized double-blind placebo-controlled trial to test the potential efficacy, assessed by improvement of oxidative-stress parameters and liver ultrasound, and tolerability of a mixture of vitamin E and Hydroxytyrosol (HXT) in adolescents with biopsy-proven NAFLD...
December 27, 2018: Antioxidants & Redox Signaling
Se-Jin Jeong, Xiangyu Zhang, Astrid Rodriguez-Velez, Trent D Evans, Babak Razani
SIGNIFICANCE: p62/SQSTM1 is a multi-functional scaffolding protein involved in the regulation of various signaling pathways as well as autophagy. In particular, p62/SQSTM1 serves as an essential adaptor to identify and deliver specific organelles and protein aggregates to autophagosomes for degradation, a process known as selective autophagy. With the emergence of autophagy as a critical process in cellular metabolism and the development of cardiometabolic diseases, it is increasingly important to understand p62's role in the integration of signaling and autophagic pathways...
December 27, 2018: Antioxidants & Redox Signaling
Yeni Kim, Krishna C Vadodaria, Zsolt Lenkei, Tadafumi Kato, Fred H Gage, Maria C Marchetto, Renata Santos
Our current knowledge of the pathophysiology and molecular mechanisms causing psychiatric disorders is modest, but genetic susceptibility and environmental factors are central to the etiology of these conditions. Autism, schizophrenia, bipolar disorder and major depressive disorder show genetic gene risk overlap and share symptoms and metabolic comorbidities. The identification of such common features may provide insights into the development of these disorders. Multiple pieces of evidence suggest that brain energy metabolism, mitochondrial functions and redox balance are impaired to various degrees in psychiatric disorders...
December 26, 2018: Antioxidants & Redox Signaling
Victor Tseng, Roy Sutliff, C Michael Hart
SIGNIFICANCE: Peroxisome proliferator-activated receptor-γ (PPARγ) maintains pulmonary vascular health through coordination of antioxidant defense systems, inflammation, and cellular metabolism. Insufficient PPARγ contributes to pulmonary hypertension (PH) pathogenesis, whereas therapeutic restoration of PPARγ activity attenuates PH in preclinical models. Recent Advances: Numerous studies in the past decade have elucidated the complex mechanisms by which PPARγ in the pulmonary vasculature and right ventricle protects against PH...
December 22, 2018: Antioxidants & Redox Signaling
Amal Kouadri, Mariam El Kathib, Johanna Cormenier, Sylvain Chauvet, Wael Zeinyeh, Micheline El Khoury, Laurence Macari, Pierre Richaud Richaud, Christelle Coraux, Isabelle Michaud-Soret, Nadia Alfaidy, Mohamed Benharouga
AIM: Bronchial epithelium acts as a defensive barrier against inhaled pollutants and microorganisms. This barrier is often compromised in inflammatory airway diseases that are characterized by excessive oxidative stress responses, leading to bronchial epithelial shedding, barrier failure, and increased bronchial epithelium permeability. Among proteins expressed in the junctional barrier and participating to the regulation of the response to oxidative and to environmental stresses is the cellular prion protein (PrPC)...
December 20, 2018: Antioxidants & Redox Signaling
Laura Weise-Cross, Thomas C Resta, Nikki L Jernigan
SIGNIFICANCE: Pulmonary hypertension is characterized by elevated vascular resistance due to vasoconstriction and remodeling of the normally low-pressure pulmonary vasculature. Redox stress contributes to the pathophysiology of this disease by altering the regulation and activity of membrane receptors, K+ channels, and intracellular Ca2+ homeostasis. Recent Advances: Antioxidant therapies have had limited success in treating pulmonary hypertension, leading to a growing appreciation that reductive stress, in addition to oxidative stress, plays a role in metabolic and cell signaling dysfunction in pulmonary vascular cells...
December 20, 2018: Antioxidants & Redox Signaling
Benjamin Marchandot, Marion Kibler, Anne Laure Charles, Annie Trinh, Helene Petit-Eisenmann, Floriane Zeyons, Jean-Jacques Von Hunolstein, Antje Reydel, Matsushita Kentsuke, Michel Kindo, Tam Hoang Minh, Pierre Leddet, Fabien De Poli, Nathan Messas, Laurence Jesel, Patrick Ohlmann, Bernard Geny, Olivier Morel
Reactive oxygen species (ROS) are central bioenergetics markers linked to aortic stenosis (AS) development and severity. We sought to evaluate the time-course and impact of ROS assessed by plasmatic superoxide anion (SA) amongst patients undergoing transcatheter aortic valve replacement (TAVR). Amongst 106 patients, SA significantly decreased after TAVR. Dropped values were measured 10 minutes after TAVR (0.590±0.181 vs 0.648±0.193; p<0.001) and persistent at 3-days (0. 611±0.0.228 vs 0.646±0.199; p=0...
December 20, 2018: Antioxidants & Redox Signaling
Wen Sun, Jie Yu, Hongwei Gao, Xiaxia Wu, Sheng Wang, Ying Hou, Jin-Jian Lu, Xiuping Chen
AIMS: Most chemotherapeutic agents exploit apoptotic signaling to trigger cancer cell death, which frequently results in drug resistance. Necroptosis, a non-apoptotic form of regulated cell death, offers an alternative strategy to eradicate apoptosis-resistant cancer cells. We previously reported a natural necroptosis inducer 2-methoxy-6-acetyl-7-methyljuglone (MAM) in A549 lung cancer cells. The current study is designed to investigate the detailed necroptotic signaling and its cytotoxicity on drug-resistant cancer cells...
December 15, 2018: Antioxidants & Redox Signaling
Mirko Zaffagnini, Simona Fermani, Christophe H Marchand, Alex Costa, Francesca Sparla, Nicolas Rouhier, Peter Geigenberger, Stéphane D Lemaire, Paolo Trost
Redox homeostasis consists of an intricate network in which reactive molecular species (RMS), redox modifications and redox proteins act in concert to allow both physiological responses and adaptation to stress conditions. This review highlights established and novel thiol-based regulatory pathways underlying the functional facets and significance of redox biology in photosynthetic organisms. This cannot be all-encompassing, but is intended to provide a comprehensive overview on the structural/molecular mechanisms governing the most relevant thiol switching modifications with emphasis on the large genetic and functional diversity of redox controllers (i...
November 30, 2018: Antioxidants & Redox Signaling
Norberto Ariel Gandini, Eliana Noelia Alonso, Maria Eugenia Fermento, Marilina Mascaró, Martin Carlos Abba, Georgina Pamela Coló, Julian Arevalo, Maria Julia Ferronato, Josefina Alejandra Guevara, Myriam Nuñez, Pamela Pichel, Alejandro Carlos Curino, María Marta Facchinetti
AIMS: Heme Oxygenase-1 (HO-1) is an enzyme involved in cellular responses to oxidative stress and has also been shown to regulate processes related to cancer progression. In this regard, HO-1 has been shown to display a dual effect with either antitumor or protumor activity, being this also true for breast cancer (BC). In this work we intended to address this discrepancy regarding the role of HO-1 in BC. RESULTS: HO-1 was detected in human breast cancer tissues, and its protein levels correlated with reduced tumor size and longer overall survival time of patients, thus suggesting the clinical importance of HO-1 in this type of cancer...
November 28, 2018: Antioxidants & Redox Signaling
Hongwei Yi, Deyi Xu, Xudong Wu, Fang Xu, Lin Lin, Huiping Zhou
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver diseases. The prevalence of NAFLD is continuously rising as the prevalence of obesity and metabolic syndrome is increasing. However, there are no approved pharmacotherapies for the treatment of NAFLD other than managing life style and controlling diets. Extensive studies have demonstrated that multiple mechanisms are involved in free fatty acid (FFA)- and high fat diet (HFD)-induced hepatic injury, including mitochondrial dysfunction, activation of oxidative stress and endoplasmic reticulum (ER) stress and lysosome dysfunction...
November 28, 2018: Antioxidants & Redox Signaling
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