3,788 results match your criteria Antioxid. Redox Signal.[Journal]


Peroxiredoxin 6 confers protection against non-alcoholic fatty liver disease through maintaining mitochondrial function.

Antioxid Redox Signal 2019 Apr 22. Epub 2019 Apr 22.

Chungbuk National University, College of Pharmacy and Medical Research Center , College of Pharmacy and Medical Research Center, Chungbuk National University, 194-31, Osongsaengmyeong 1-ro, Osong-eup, Cheongwon-gun,Chungbuk, Republic of Korea, 361-951. , Osong-eup, Korea (the Republic of) , 361-951 ;

Aim: Non-alcoholic fatty liver disease (NAFLD) accompanies by excessive reactive oxygen species (ROS) production, which has been suggested in several studies to link with mitochondrial function. However, the mechanistic role of ROS-mediated regulation of mitochondrial function in NAFLD has not been elucidated. Since peroxiredoxin 6 (PRDX6) is an only member of the antioxidant PRDX family that translocates to damaged mitochondria, we investigated the PRDX6-mediated anti-steatotic mechanism using genetic modified mice and cells. Read More

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http://dx.doi.org/10.1089/ars.2018.7544DOI Listing

The role of mitochondrial and endoplasmic reticulum ROS production in models of perinatal brain injury.

Antioxid Redox Signal 2019 Apr 8. Epub 2019 Apr 8.

University of Gothenburg, 3570, Centre of Perinatal Medicine and Health, Sahlgrenska Academy, Gothenburg, Sweden.

Significance: Perinatal brain injury is caused by hypoxia-ischemia (HI) in term neonates, perinatal arterial stroke, and infection/inflammation leading to devastating long-term neurodevelopmental deficits. Therapeutic hypothermia is the only currently available treatment but is not successful in more than 50% of term neonates suffering from hypoxic-ischemic encephalopathy. Thus, there is an urgent unmet need for alternative or adjunct therapies. Read More

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http://dx.doi.org/10.1089/ars.2019.7779DOI Listing
April 2019
1 Read

Inhibitory Effect of Sestrin2 on Hepatic Stellate Cell Activation and Liver Fibrosis via Blocking Transforming Growth Factor-β Signaling.

Antioxid Redox Signal 2019 Mar 26. Epub 2019 Mar 26.

Chosun University, College of Pharmacy , 375 Seosuk-dong , Donggu , Gwangju, Korea, Republic of ;

Aims: Hepatic fibrosis results from chronic liver injury and inflammatory responses. Sestrin2 (Sesn2), an evolutionarily conserved antioxidant enzyme, reduces the severities of acute hepatitis and metabolic liver diseases. However, the role of Sesn2 in the pathogenesis of liver fibrosis remains obscure. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7559
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http://dx.doi.org/10.1089/ars.2018.7559DOI Listing
March 2019
3 Reads

Mitochondrial Reactive Oxygen Species Generated at the Complex-II Matrix or Intermembrane Space Microdomain Have Distinct Effects on Redox Signaling and Stress Sensitivity in .

Antioxid Redox Signal 2019 Apr 22. Epub 2019 Apr 22.

1 Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, New York.

How mitochondrial reactive oxygen species (ROS) impact physiological function may depend on the quantity of ROS generated or removed, and the subcellular microdomain in which this occurs. However, pharmacological tools currently available to alter ROS production lack precise spatial and temporal control. We used CRISPR/Cas9 to fuse the light-sensitive ROS-generating protein, SuperNova to the C-terminus of mitochondrial complex II succinate dehydrogenase subunits B (SDHB-1::SuperNova) and C (SDHC-1::SuperNova) in to localize SuperNova to the matrix-side of the inner mitochondrial membrane, and to the intermembrane space (IMS), respectively. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7681
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http://dx.doi.org/10.1089/ars.2018.7681DOI Listing
April 2019
3 Reads

Quantitative analyses of the yeast oxidative protein folding pathway and .

Antioxid Redox Signal 2019 Mar 18. Epub 2019 Mar 18.

School of Biosciences , University of Kent , Canterbury, Kent, United Kingdom of Great Britain and Northern Ireland , CT2 7NJ ;

Aims: Efficient oxidative protein folding (OPF) in the endoplasmic reticulum (ER) is a key requirement of the eukaryotic secretory pathway. In particular, protein folding linked to the formation of disulfide bonds, an activity dependent on the enzyme protein disulfide isomerase (PDI), is crucial. For the de novo formation of disulphide bonds, reduced PDI must be re-oxidised by an ER-located oxidase (ERO1). Read More

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http://dx.doi.org/10.1089/ars.2018.7615DOI Listing
March 2019
2 Reads

Which antioxidant system shapes intracellular H2O2 gradients?

Antioxid Redox Signal 2019 Mar 13. Epub 2019 Mar 13.

Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow, Russian Federation.

Cellular antioxidant systems control the levels of hydrogen peroxide (H2O2) within cells. Multiple theoretical models exist that predict the diffusion properties of H2O2 depending on the rate of H2O2 generation and amount and reaction rates of antioxidant machinery components. Despite these theoretical predictions, it has remained unknown how antioxidant systems shape intracellular H2O2 gradients. Read More

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http://dx.doi.org/10.1089/ars.2018.7697DOI Listing

Metallothionein Protects the Heart Against Myocardial Infarction via the mTORC2/FoxO3a/Bim Pathway.

Antioxid Redox Signal 2019 Apr 11. Epub 2019 Apr 11.

2 School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, People's Republic of China.

Aims: Cardiac-specific overexpression of metallothionein (MT) has been shown to be beneficial in ischemic heart disease, but the detailed mechanisms through which MT protects against myocardial infarction (MI) remain unknown. This study assessed the involvement of the mTORC2/FoxO3a/Bim pathway in the cardioprotective effects of MT.

Results: MI was induced in wild-type (FVB) mice and in cardiac-specific MT-overexpressing transgenic (MT-TG) mice by ligation of the left anterior descending (LAD) coronary artery. Read More

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http://dx.doi.org/10.1089/ars.2018.7597DOI Listing

Human Embryonic Stem Cell-Derived Cardiovascular Progenitors Repair Infarcted Hearts Through Modulation of Macrophages via Activation of Signal Transducer and Activator of Transcription 6.

Antioxid Redox Signal 2019 Apr 16. Epub 2019 Apr 16.

1 CAS Key Laboratory of Tissue Microenvironment and Tumor, Laboratory of Molecular Cardiology, Shanghai Jiao Tong University School of Medicine and Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences (CAS), Chinese Academy of Sciences, Shanghai, People's Republic of China.

Aims: Human embryonic stem cell derived-cardiovascular progenitor cells (hESC-CVPCs) are a promising cell source for cardiac repair, while the underlying mechanisms need to be elucidated. We recently observed cardioprotective effects of human pluripotent stem cell (hPSC)-CVPCs in infarcted nonhuman primates, but their effects on inflammation during early phase of myocardial infarction (MI) and the contribution of such effect to the cardioprotection are unclear.

Results: Injection of hESC-CVPCs into acutely infarcted myocardium significantly ameliorated the functional worsening and scar formation, concomitantly with reduced inflammatory reactions and cardiomyocyte apoptosis as well as increased vascularization. Read More

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http://dx.doi.org/10.1089/ars.2018.7688DOI Listing

Peroxisome Proliferator-Activated Receptor-γ Coactivator-1α Inhibits Vascular Calcification Through Sirtuin 3-Mediated Reduction of Mitochondrial Oxidative Stress.

Antioxid Redox Signal 2019 Apr 2. Epub 2019 Apr 2.

1 Department of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, and Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.

Aims: Vascular calcification is associated with cardiovascular death in patients with chronic kidney disease (CKD). Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) plays an important role in various cardiovascular diseases. However, its role in vascular calcification remains unknown. Read More

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http://dx.doi.org/10.1089/ars.2018.7620DOI Listing
April 2019
7.407 Impact Factor

Putative Role of Nuclear Factor-Kappa B But Not Hypoxia-Inducible Factor-1α in Hypoxia-Dependent Regulation of Oxidative Stress in Hematopoietic Stem and Progenitor Cells.

Antioxid Redox Signal 2019 Apr 10. Epub 2019 Apr 10.

1 Experimental Hematology Unit, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.

Aims: Adaptation to low oxygen of hematopoietic stem cells (HSCs) in the bone marrow has been demonstrated to depend on the activation of hypoxia-inducible factor (HIF)-1α as well as the limited production of reactive oxygen species (ROS). In this study, we aimed at determining whether HIF-1α is involved in protecting HSCs from ROS.

Results: Oxidative stress was induced by DL-buthionine-(S,R)-sulfoximine (BSO)-treatment, which increases the mitochondrial ROS level. Read More

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http://dx.doi.org/10.1089/ars.2018.7551DOI Listing

HIF-1α Preconditioning Potentiates Antioxidant Activity in Ischemic Injury: The Role of Sequential Administration of Dihydrotanshinone I and Protocatechuic Aldehyde in Cardioprotection.

Antioxid Redox Signal 2019 Apr 3. Epub 2019 Apr 3.

1 State Key Laboratory of Natural Medicines, Department of Pharmacognosy, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing, China.

Aims: The management of myocardial ischemia has been challenged by reperfusion injury. Reactive oxygen species (ROS) production is the critical cause of reperfusion injury, but antioxidant treatment failed to gain satisfactory effects. We hypothesized that improvement of redox homeostasis by preconditioning regulation should potentiate the ability of antioxidants to protect the heart from reperfusion injury. Read More

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http://dx.doi.org/10.1089/ars.2018.7624DOI Listing
April 2019
1 Read

Peroxiredoxins and Beyond; Redox Systems Regulating Lung Physiology and Disease.

Antioxid Redox Signal 2019 Apr 5. Epub 2019 Apr 5.

Department of Pathology and Laboratory Medicine, Larner College of Medicine, University of Vermont, Burlington, Vermont.

Significance: The lung is a unique organ, as it is constantly exposed to air, and thus it requires a robust antioxidant defense system to prevent the potential damage from exposure to an array of environmental insults, including oxidants. The peroxiredoxin (PRDX) family plays an important role in scavenging peroxides and is critical to the cellular antioxidant defense system. Recent Advances: Exciting discoveries have been made to highlight the key features of PRDXs that regulate the redox tone. Read More

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http://dx.doi.org/10.1089/ars.2019.7752DOI Listing
April 2019
1 Read

Redox Imbalance in Idiopathic Pulmonary Fibrosis: A Role for Oxidant Cross-Talk Between NADPH Oxidase Enzymes and Mitochondria.

Antioxid Redox Signal 2019 Apr 5. Epub 2019 Apr 5.

2 Department of Pathology and Laboratory Medicine, Larner College of Medicine, University of Vermont, Burlington, Vermont.

Significance: Idiopathic pulmonary fibrosis (IPF) is a progressive age-related lung disease with a median survival of only 3 years after diagnosis. The pathogenic mechanisms behind IPF are not clearly understood, and current therapeutic approaches have not been successful in improving disease outcomes. Recent Advances: IPF is characterized by increased production of reactive oxygen species (ROS), primarily by NADPH oxidases (NOXes) and mitochondria, as well as altered antioxidant defenses. Read More

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http://dx.doi.org/10.1089/ars.2019.7742DOI Listing
April 2019
5 Reads

Cellular Compartmentation and the Redox/Nonredox Functions of NAD.

Antioxid Redox Signal 2019 Mar 26. Epub 2019 Mar 26.

Department of Anesthesiology, University of Rochester Medical Center, Rochester, New York.

Significance: Nicotinamide adenine dinucleotide (NAD) spans diverse roles in biology, serving as both an important redox cofactor in metabolism and a substrate for signaling enzymes that regulate protein post-translational modifications (PTMs).

Critical Issues: Although the interactions between these different roles of NAD (and its reduced form NADH) have been considered, little attention has been paid to the role of compartmentation in these processes. Specifically, the role of NAD in metabolism is compartment specific (e. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7722
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http://dx.doi.org/10.1089/ars.2018.7722DOI Listing
March 2019
4 Reads

Galectin-3: A Harbinger of Reactive Oxygen Species, Fibrosis, and Inflammation in Pulmonary Arterial Hypertension.

Antioxid Redox Signal 2019 Mar 29. Epub 2019 Mar 29.

1 Department of Pharmacology and Toxicology, Medical College of Georgia at Augusta University, Augusta, Georgia.

Significance: Pulmonary arterial hypertension (PAH) is a progressive disease arising from the narrowing of pulmonary arteries (PAs) resulting in high pulmonary arterial blood pressure and ultimately right ventricle (RV) failure. A defining characteristic of PAH is the excessive and unrelenting inward remodeling of PAs 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. Read More

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http://dx.doi.org/10.1089/ars.2019.7753DOI Listing

Gender Difference in Damage-Mediated Signaling Contributes to Pulmonary Arterial Hypertension.

Antioxid Redox Signal 2019 Mar 20. Epub 2019 Mar 20.

1 Division of Endocrinology, University of Arizona, Tucson, Arizona.

Aims: Pulmonary arterial hypertension (PAH) is a progressive lethal disease with a known gender dimorphism. Female patients are more susceptible to PAH, whereas male patients have a lower survival rate. Initial pulmonary vascular damage plays an important role in PAH pathogenesis. Read More

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http://dx.doi.org/10.1089/ars.2018.7664DOI Listing
March 2019
7.407 Impact Factor

Selenoprotein M Promotes Hypothalamic Leptin Signaling and Thioredoxin Antioxidant Activity.

Antioxid Redox Signal 2019 Mar 6. Epub 2019 Mar 6.

2 Department of Cell and Molecular Biology, and Medical Microbiolgy, and Pharmacology, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii.

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 endoplasmic reticulum (ER)-resident oxidoreductase bearing structural similarity to thioredoxin (TXN), is among those yet to be fully characterized. Read More

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http://dx.doi.org/10.1089/ars.2018.7594DOI Listing

Thiol-Redox Regulation in Lung Development and Vascular Remodeling.

Antioxid Redox Signal 2019 Mar 5. Epub 2019 Mar 5.

Redox Biology Laboratory, Division of Neonatology, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama.

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. Read More

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http://dx.doi.org/10.1089/ars.2018.7712DOI Listing

Biomechanical Forces and Oxidative Stress: Implications for Pulmonary Vascular Disease.

Antioxid Redox Signal 2019 Mar 19. Epub 2019 Mar 19.

1 Department of Medicine, The University of Arizona Health Sciences, Tucson, Arizona.

Significance: Oxidative stress in the cell is characterized by excessive generation of reactive oxygen species (ROS). Superoxide (O) and hydrogen peroxide (HO) are the main ROS involved in the regulation of cellular metabolism. As our fundamental understanding of the underlying causes of lung disease has increased it has become evident that oxidative stress plays a critical role. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7720
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http://dx.doi.org/10.1089/ars.2018.7720DOI Listing
March 2019
15 Reads

Crosstalk Between Mitochondrial Hyperacetylation and Oxidative Stress in Vascular Dysfunction and Hypertension.

Antioxid Redox Signal 2019 Feb 28. Epub 2019 Feb 28.

Department of Medicine, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee.

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. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7632
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http://dx.doi.org/10.1089/ars.2018.7632DOI Listing
February 2019
9 Reads

Bioenergetic Differences in the Airway Epithelium of Lean Versus Obese Asthmatics Are Driven by Nitric Oxide and Reflected in Circulating Platelets.

Antioxid Redox Signal 2019 Mar 6. Epub 2019 Mar 6.

2 Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.

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 asthma pathogenesis, it is unclear whether these mechanisms differ in lean versus obese asthmatics. In addition, we previously demonstrated that circulating platelets from asthmatic individuals have altered bioenergetics; however, it is unknown whether platelet mitochondrial changes reflect those observed in airway epithelial cells. Read More

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http://dx.doi.org/10.1089/ars.2018.7627DOI Listing

Mitochondrial Dysfunction: Metabolic Drivers of Pulmonary Hypertension.

Antioxid Redox Signal 2019 Feb 25. Epub 2019 Feb 25.

2 Department of Pediatrics, Cardiovascular Pulmonary Research Labs and Pediatric Critical Care Medicine, University of Colorado Denver, Aurora, Colorado.

Significance: 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 overall survival rate is ranging from 28-72%. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7705
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http://dx.doi.org/10.1089/ars.2018.7705DOI Listing
February 2019
5 Reads

The Antioxidant Effects of Hydroxytyrosol and Vitamin E on Pediatric Nonalcoholic Fatty Liver Disease, in a Clinical Trial: A New Treatment?

Antioxid Redox Signal 2019 Feb 11. Epub 2019 Feb 11.

5 Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.

Nonalcoholic 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 pediatric nonalcoholic steatohepatitis. 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. Read More

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http://dx.doi.org/10.1089/ars.2018.7704DOI Listing
February 2019
1 Read

p62/SQSTM1 and Selective Autophagy in Cardiometabolic Diseases.

Antioxid Redox Signal 2019 Feb 11. Epub 2019 Feb 11.

1 Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.

Significance: p62/SQSTM1 is a multifunctional 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.

Critical Issues: 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. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7649
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http://dx.doi.org/10.1089/ars.2018.7649DOI Listing
February 2019
11 Reads

Mitochondria, Metabolism, and Redox Mechanisms in Psychiatric Disorders.

Antioxid Redox Signal 2019 Feb 1. Epub 2019 Feb 1.

2 Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California.

Significance: 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. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7606
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http://dx.doi.org/10.1089/ars.2018.7606DOI Listing
February 2019
9 Reads

Redox Biology of Peroxisome Proliferator-Activated Receptor-γ in Pulmonary Hypertension.

Antioxid Redox Signal 2019 Feb 25. Epub 2019 Feb 25.

1 Department of Medicine, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Emory University, Atlanta, Georgia.

Significance: Peroxisome proliferator-activated receptor-gamma (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 (RV) protects against PH. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7695
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http://dx.doi.org/10.1089/ars.2018.7695DOI Listing
February 2019
7 Reads

Involvement of the Prion Protein in the Protection of the Human Bronchial Epithelial Barrier Against Oxidative Stress.

Antioxid Redox Signal 2019 Feb 4. Epub 2019 Feb 4.

1 University of Grenoble Alpes, CNRS, UMR 5249, CEA, BIG, CBM, Grenoble, France.

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 (PrP). Read More

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http://dx.doi.org/10.1089/ars.2018.7500DOI Listing
February 2019
4 Reads
7.407 Impact Factor

Redox Regulation of Ion Channels and Receptors in Pulmonary Hypertension.

Antioxid Redox Signal 2019 Jan 25. Epub 2019 Jan 25.

Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.

Significance: Pulmonary hypertension (PH) 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 Ca homeostasis. Recent Advances: Antioxidant therapies have had limited success in treating PH, 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. Read More

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http://dx.doi.org/10.1089/ars.2018.7699DOI Listing
January 2019

Does Transcatheter Aortic Valve Replacement Modulate the Kinetic of Superoxide Anion Generation?

Antioxid Redox Signal 2019 Jan 31. Epub 2019 Jan 31.

1 Pôle d'Activité Médico-Chirurgicale Cardio-Vasculaire, Nouvel Hôpital Civil, Centre Hospitalier Universitaire, Université de Strasbourg, Strasbourg, France.

Reactive oxygen species (ROS) are central bioenergetic 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) among patients undergoing transcatheter aortic valve replacement (TAVR). Among 106 patients, SA significantly decreased after TAVR. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7689
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http://dx.doi.org/10.1089/ars.2018.7689DOI Listing
January 2019
18 Reads

Inhibition of Lung Cancer by 2-Methoxy-6-Acetyl-7-Methyljuglone Through Induction of Necroptosis by Targeting Receptor-Interacting Protein 1.

Antioxid Redox Signal 2019 Feb 1. Epub 2019 Feb 1.

1 State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Taipa, China.

Aims: Most chemotherapeutic agents exploit apoptotic signaling to trigger cancer cell death, which frequently results in drug resistance. Necroptosis, a nonapoptotic 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. Read More

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http://dx.doi.org/10.1089/ars.2017.7376DOI Listing
February 2019
3 Reads

Redox Homeostasis in Photosynthetic Organisms: Novel and Established Thiol-Based Molecular Mechanisms.

Antioxid Redox Signal 2019 Feb 25. Epub 2019 Feb 25.

1 Department of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy.

Significance: Redox homeostasis consists of an intricate network of reactions in which reactive molecular species, redox modifications, and redox proteins act in concert to allow both physiological responses and adaptation to stress conditions. Recent Advances: This review highlights established and novel thiol-based regulatory pathways underlying the functional facets and significance of redox biology in photosynthetic organisms. In the last decades, the field of redox regulation has largely expanded and this work is aimed at giving the right credit to the importance of thiol-based regulatory and signaling mechanisms in plants. Read More

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http://dx.doi.org/10.1089/ars.2018.7617DOI Listing
February 2019

Heme Oxygenase-1 Has an Antitumor Role in Breast Cancer.

Antioxid Redox Signal 2019 Jan 25. Epub 2019 Jan 25.

1 Laboratorio de Biología del Cáncer, Instituto de Investigaciones Bioquímicas de Bahía Blanca (INIBIBB), Universidad Nacional del Sur (UNS)-CONICET, Dpto. de Biología, Bioquímica y Farmacia (UNS), Bahía Blanca, Argentina.

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, which is also true for breast cancer (BC). In this work, we address this discrepancy regarding the role of HO-1 in BC. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7554
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http://dx.doi.org/10.1089/ars.2018.7554DOI Listing
January 2019
3 Reads

Isosteviol Protects Free Fatty Acid- and High Fat Diet-Induced Hepatic Injury via Modulating PKC-β/p66Shc/ROS and Endoplasmic Reticulum Stress Pathways.

Antioxid Redox Signal 2019 Jan 28. Epub 2019 Jan 28.

3 Department of Microbiology and Immunology, Virginia Commonwealth University and McGuire Veterans Affairs Medical Center, Richmond, Virginia.

Aims: Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver diseases. 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. Read More

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http://dx.doi.org/10.1089/ars.2018.7521DOI Listing
January 2019

Contribution of Oxidative Stress and Impaired Biogenesis of Pancreatic β-Cells to Type 2 Diabetes.

Antioxid Redox Signal 2019 Jan 24. Epub 2019 Jan 24.

Department of Mitochondrial Physiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.

Significance: Type 2 diabetes development involves multiple changes in β-cells, related to the oxidative stress and impaired redox signaling, beginning frequently by sustained overfeeding due to the resulting lipotoxicity and glucotoxicity. Uncovering relationships among the dysregulated metabolism, impaired β-cell "well-being," biogenesis, or cross talk with peripheral insulin resistance is required for elucidation of type 2 diabetes etiology. Recent Advances: It has been recognized that the oxidative stress, lipotoxicity, and glucotoxicity cannot be separated from numerous other cell pathology events, such as the attempted compensation of β-cell for the increased insulin demand and dynamics of β-cell biogenesis and its "reversal" at dedifferentiation, that is, from the concomitantly decreasing islet β-cell mass (also due to transdifferentiation) and low-grade islet or systemic inflammation. Read More

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http://dx.doi.org/10.1089/ars.2018.7656DOI Listing
January 2019
1 Read

NADPH Oxidase 4 Regulates Inflammation in Ischemic Heart Failure: Role of Soluble Epoxide Hydrolase.

Antioxid Redox Signal 2018 Dec 28. Epub 2018 Dec 28.

1 Frankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan.

Aims: Oxidative stress is implicated in cardiomyocyte cell death and cardiac remodeling in the failing heart. The role of NADPH oxidase 4 (NOX4) in cardiac adaptation to pressure overload is controversial, but its function in myocardial ischemic stress has not been thoroughly elucidated. This study examined the function of NOX4 in the pathogenesis of ischemic heart failure, utilizing mouse models, cell culture, and human heart samples. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7548
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http://dx.doi.org/10.1089/ars.2018.7548DOI Listing
December 2018
19 Reads

Redox- and Ligand Binding-Dependent Conformational Ensembles in the Human Apoptosis-Inducing Factor Regulate Its Pro-Life and Cell Death Functions.

Antioxid Redox Signal 2019 Jan 11. Epub 2019 Jan 11.

1 Departamento de Bioquímica y Biología Molecular y Celular, Facultad de Ciencias, Instituto de Biocomputación y Física de Sistemas Complejos (GBsC-CSIC and BIFI-IQFR Joint Units), Universidad de Zaragoza, Zaragoza, Spain.

Aims: The human apoptosis-inducing factor (hAIF) supports OXPHOS biogenesis and programmed cell death, with missense mutations producing neurodegenerative phenotypes. hAIF senses the redox environment of cellular compartments, stabilizing a charge transfer complex (CTC) dimer that modulates the protein interaction network. In this context, we aimed to evaluate the subcellular pH, CTC formation, and pathogenic mutations effects on hAIF stability, and a thermal denaturation high-throughput screening (HTS) assay to discover AIF binders. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7658
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http://dx.doi.org/10.1089/ars.2018.7658DOI Listing
January 2019
13 Reads

Nitrite Protects Neurons Against Hypoxic Damage Through S-nitrosylation of Caspase-6.

Antioxid Redox Signal 2018 Dec 28. Epub 2018 Dec 28.

1 Institute of Biochemical Sciences, National Taiwan University, Taipei, Taiwan.

Aims: The coordination of neurons to execute brain functions requires plenty of oxygen. Thus, it is not surprising that the chronic hypoxia resulting from chronic obstructive pulmonary diseases (COPD) can cause neuronal damage. Injury in the cortex can give rise to anxiety and cognitive dysfunction. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7522
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http://dx.doi.org/10.1089/ars.2018.7522DOI Listing
December 2018
14 Reads

Myocardial Energy Stress, Autophagy Induction, and Cardiomyocyte Functional Responses.

Antioxid Redox Signal 2019 Jan 10. Epub 2019 Jan 10.

2 Department of Physiology, University of Melbourne, Melbourne, Australia.

Significance: Energy stress in the myocardium occurs in a variety of acute and chronic pathophysiological contexts, including ischemia, nutrient deprivation, and diabetic disease settings of substrate disturbance. Although the heart is highly adaptive and flexible in relation to fuel utilization and routes of adenosine-5'-triphosphate (ATP) generation, maladaptations in energy stress situations confer functional deficit. An understanding of the mechanisms that link energy stress to impaired myocardial performance is crucial. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7650
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http://dx.doi.org/10.1089/ars.2018.7650DOI Listing
January 2019
15 Reads

Metabolic Resuscitation Strategies to Prevent Organ Dysfunction in Sepsis.

Antioxid Redox Signal 2019 Jan 24. Epub 2019 Jan 24.

1 Department of Clinical Pharmacy and Pharmacology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.

Significance: Sepsis is the main cause of death among patients admitted to the intensive care unit. As current treatment is limited to antimicrobial therapy and supportive care, mortality remains high, which warrants efforts to find novel therapies. Recent Advances: Mitochondrial dysfunction is emerging as a key process in the induction of organ dysfunction during sepsis, and metabolic resuscitation might reveal to be a novel cornerstone in the treatment of sepsis. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7537
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http://dx.doi.org/10.1089/ars.2018.7537DOI Listing
January 2019
14 Reads

Nuclear Factor (Erythroid-Derived 2)-Like 2 Regulates the Hepatoprotective Effects of Remote Ischemic Conditioning in Hemorrhagic Shock.

Antioxid Redox Signal 2019 May 20;30(14):1760-1773. Epub 2018 Dec 20.

1 Department of Surgery, St. Michael's Hospital, Toronto, Ontario, Canada.

Aims: Remote ischemic conditioning (RIC) protects against organ ischemia/reperfusion injury in experimental and clinical settings. We have demonstrated that RIC prevents liver and lung inflammation/injury after hemorrhagic shock/resuscitation (S/R). In this study, we used a murine model of S/R to investigate the role of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in mediating hepatoprotection. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7541
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May 2019
20 Reads

Metabolism and Redox in Pulmonary Vascular Physiology and Pathophysiology.

Antioxid Redox Signal 2018 Dec 21. Epub 2018 Dec 21.

Department of Physiology, New York Medical College , Valhalla, New York.

Significance: This review considers how some systems controlling pulmonary vascular function are potentially regulated by redox processes to examine how and why conditions such as prolonged hypoxia, pathological mediators, and other factors promoting vascular remodeling contribute to the development of pulmonary hypertension (PH). Recent Advances and Critical Issues: Aspects of vascular remodeling induction mechanisms described are associated with shifts in glucose metabolism through the pentose phosphate pathway and increased cytosolic NADPH generation by glucose-6-phosphate dehydrogenase, increased glycolysis generation of cytosolic NADH and lactate, mitochondrial dysfunction associated with superoxide dismutase-2 depletion, changes in reactive oxygen species and iron metabolism, and redox signaling.

Future Directions: The regulation and impact of hypoxia-inducible factor and the function of cGMP-dependent and redox regulation of protein kinase G are considered for their potential roles as key sensors and coordinators of redox and metabolic processes controlling the progression of vascular pathophysiology in PH, and how modulating aspects of metabolic and redox regulatory systems potentially function in beneficial therapeutic approaches. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7657
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http://dx.doi.org/10.1089/ars.2018.7657DOI Listing
December 2018
16 Reads

Quantitative Real-Time Imaging of Glutathione with Subcellular Resolution.

Antioxid Redox Signal 2019 Jun 20;30(16):1900-1910. Epub 2018 Dec 20.

1 Department of Pharmacology and Chemical Biology,Baylor College of Medicine, Houston, Texas.

Aims: Quantitative imaging of glutathione (GSH) with high spatial and temporal resolution is essential for studying the roles of GSH in redox biology. To study the long-standing question of compartmentalization of GSH, especially its distribution between the nucleus and cytosol, an organelle-targeted quantitative probe is needed.

Results: We developed a reversible reaction-based ratiometric fluorescent probe-HaloRT-that can quantitatively measure GSH dynamics with subcellular resolution in real time. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7605
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http://dx.doi.org/10.1089/ars.2018.7605DOI Listing
June 2019
15 Reads

Aanat knockdown and melatonin supplementation in embryo development: involvement of mitochondrial function and DNA methylation.

Antioxid Redox Signal 2018 Oct 20. Epub 2018 Oct 20.

college of animal science and technology , China Agricultural University, Beijing, 100193, China , Beijing, China , 100193 ;

Aims: In addition to pineal gland, many cells, tissues and organs also synthesize melatonin. Embryos are group of special cells whether they can synthesize melatonin is still an open question. However, melatonin application promoted embryo development in many species under the in vitro condition. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7555
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http://dx.doi.org/10.1089/ars.2018.7555DOI Listing
October 2018
11 Reads

Vascular Biology of Superoxide-Generating NADPH Oxidase 5-Implications in Hypertension and Cardiovascular Disease.

Antioxid Redox Signal 2019 Mar 15;30(7):1027-1040. Epub 2018 Nov 15.

BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.

Significance: NADPH oxidases (Noxs), of which there are seven isoforms (Nox1-5, Duox1/Duox2), are professional oxidases functioning as reactive oxygen species (ROS)-generating enzymes. ROS are signaling molecules important in physiological processes. Increased ROS production and altered redox signaling in the vascular system have been implicated in the pathophysiology of cardiovascular diseases, including hypertension, and have been attributed, in part, to increased Nox activity. Read More

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http://dx.doi.org/10.1089/ars.2018.7583DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6354601PMC
March 2019
1 Read

Transient Receptor Potential Canonical 3 and Nuclear Factor of Activated T Cells C3 Signaling Pathway Critically Regulates Myocardial Fibrosis.

Antioxid Redox Signal 2019 Jun 29;30(16):1851-1879. Epub 2018 Nov 29.

1 Laboratoire de Recherche en Physiologie et Physiopathologie, Pôle Technologie Santé, Faculté de Médecine, Université Saint Joseph, Beirut, Lebanon.

Aims: Cardiac fibroblasts (CFs) are emerging as major contributors to myocardial fibrosis (MF), a final common pathway of many etiologies of heart disease. Here, we studied the functional relevance of transient receptor potential canonical 3 (TRPC3) channels and nuclear factor of activated T cells c3 (NFATc3) signaling in rodent and human ventricular CFs, and whether their modulation would limit MF.

Results: A positive feedback loop between TRPC3 and NFATc3 drove a rat ventricular CF fibrotic phenotype. Read More

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https://www.liebertpub.com/doi/10.1089/ars.2018.7545
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http://dx.doi.org/10.1089/ars.2018.7545DOI Listing
June 2019
3 Reads

Mitochondrial Morphofunction in Mammalian Cells.

Antioxid Redox Signal 2018 Nov 29. Epub 2018 Nov 29.

Department of Biochemistry (286), Radboud Institute for Molecular Life Sciences, Radboud University Medical Centre, Nijmegen, The Netherlands.

Significance: In addition to their classical role in cellular ATP production, mitochondria are of key relevance in various (patho)physiological mechanisms including second messenger signaling, neuro-transduction, immune responses and death induction. Recent Advances: Within cells, mitochondria are motile and display temporal changes in internal and external structure ("mitochondrial dynamics"). During the last decade, substantial empirical and in silico evidence was presented demonstrating that mitochondrial dynamics impacts on mitochondrial function and vice versa. Read More

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http://dx.doi.org/10.1089/ars.2018.7534DOI Listing
November 2018
16 Reads

Redox Regulation of Calpains: Consequences on Vascular Function.

Antioxid Redox Signal 2019 Mar 15;30(7):1011-1026. Epub 2018 Nov 15.

1 Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany.

Significance: Calpains (CAPNs) are a family of calcium-activated cysteine proteases. The ubiquitous isoforms CAPN1 and CAPN2 have been involved in the maintenance of vascular integrity, but uncontrolled CAPN activation plays a role in the pathogenesis of vascular diseases. Recent Advances: It is well accepted that chronic and acute overproduction of reactive oxygen species (ROS) is associated with the development of vascular diseases. Read More

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http://dx.doi.org/10.1089/ars.2018.7607DOI Listing
March 2019
12 Reads

Cellular Redox Compartments.

Authors:
Thomas Kietzmann

Antioxid Redox Signal 2019 Jan 30;30(1):1-4. Epub 2018 Oct 30.

Faculty of Biochemistry and Molecular Medicine, and Biocenter Oulu, University of Oulu , Oulu, Finland .

Although initially considered as harmful, reactive oxygen species (ROS) are now also recognized as important signaling molecules affecting various cellular processes. For example, they contribute to the response to hormones, growth factors, or hypoxia, and defense reactions against mechanical or chemical stress. Therefore, different ROS-generating, ROS-utilizing, and ROS-degrading systems in different intracellular compartments play an important role. Read More

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http://dx.doi.org/10.1089/ars.2018.7661DOI Listing
January 2019

Redox Pioneer: Professor Hideo Kimura.

Authors:
David Lefer

Antioxid Redox Signal 2019 May 1;30(14):1699-1708. Epub 2018 Nov 1.

CV Center of Excellence, Louisiana State University Health Sciences Center , New Orleans, Louisiana.

Dr. Hideo Kimura is recognized as a redox pioneer because he has published an article in the field of antioxidant and redox biology that has been cited >1000 times, and 29 articles that have been cited >100 times. Since the first description of hydrogen sulfide (HS) as a toxic gas 300 years ago, most studies have been devoted to its toxicity. Read More

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http://dx.doi.org/10.1089/ars.2018.7618DOI Listing