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Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain
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Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain
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Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain
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Department of Genetics, Universitat de València, Valencia, Spain
INCLIVA Biomedical Research Institute, Unversitat de València, Valencia, Spain
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Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Valencia, Spain
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mitigation of oxidative stress to achieve the increased glutamate uptake, suggesting that neuroprotection could only be provided by targeting both aspects as a single unit ( Wilkie et al. 2021 ). In light of their great importance, an overview of the main
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Animal Science Department, Plants for Human Health Institute, North Carolina State University, Kannapolis Research Campus, Kannapolis, North Carolina, USA
Department of Food and Nutrition, Kyung Hee University, Seoul, South Korea
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energetic condition ( Imai et al. 2000 ). Not only this, SIRTs play critical roles in the regulation of cellular homeostasis, in particular oxidative stress, inflammation, metabolism and senescence ( Vachharajani et al. 2016 , Singh et al. 2018 , Lee
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liver regeneration after PHx requires NRF2, since its inactivation leads to oxidative stress-related insulin resistance, impairing the activation of anti-apoptotic and pro-mitogenic pathways ( Beyer et al. 2008 ). Of interest, NRF2 is dynamically
Department of Discovery Protein Science, Amgen Inc., South San Francisco, California, USA
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Department of Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA
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University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
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cells from ROS leaks by maintaining ER membrane integrity ( Kanekura et al. 2015 ). Oxidative stress can also directly modify IRE1α’s cysteine 663 residue in the kinase activation loop through sulfenylation ( Hourihan et al. 2016 ), attenuating its
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Trichothiodystrophy (TTD) is a rare hereditary disease whose prominent feature is brittle hair. Additional clinical signs are physical and neurodevelopmental abnormalities and in about half of the cases hypersensitivity to UV radiation. Although the mutations involved in this condition have been characterized, the correlation between the molecular defects and the plethora of clinical symptoms is not well understood. Recently the presence of a redox unbalance in TTD has been suggested although not clear evidences have been reported on this aspect.
Therefore, in the present study, we evaluated the redox status of fibroblasts isolated from a TTD patient. In addition, to understand the ability of TTD cells to respond to oxidative insults, the cells were challenged with H2O2 and mitochondrial O2- and mitochondrial membrane potential were measured in different oxidative conditions. In addition, NRF2/BACH protein levels were also analysed in response to H2O2.
The results suggested an aberrant mitochondrial response to oxidative stimuli, an increased baseline oxidative stress status in TTD and an altered NRF2/BACH level.
This study emphasises that altered redox homeostasis might play a role in TTD pathogenesis and mitochondria functionality could represent an alternative therapeutic target for this condition to improve patients clinical features.
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Experimental Medicine consists of a number of invited review papers focusing on the redox aspects of a large variety of human pathological disorders, associated with oxidative stress, like the involvement of oxidant species in the early attempt of the organism
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electrons between molecules, and maintaining their balance is essential for cellular health and function. With age, these processes tend to become dysregulated, leading to increased oxidative stress and damage, which are associated with age-related diseases
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Department of Physiology, University of Valencia, Valencia, Spain
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CIBERehd – Department of Pharmacology, University of Valencia, Valencia, Spain
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Department of Physiology, University of Valencia, Valencia, Spain
CIBERehd – Department of Pharmacology, University of Valencia, Valencia, Spain
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, causing oxidative stress. There are several pathways of ROS overproduction in T2D, which can be divided into cytoplasmic pathways and mitochondrial pathways. The first group includes the activation of NAPDH oxidases, the polyol pathway, and the enzyme
Division of Cardiology, Department of Medical Sciences, University of Turin, Italy
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, particularly HF with preserved ejection fraction (HFpEF), cardiac amyloidosis (CA) is highlighted by the likely important role that oxidative stress has in its pathogenesis and disease progression. Its main feature is the accumulation of amyloid fibrils in the
Anatomy unit, Nursing Science Department, Elizade University, Ilara-Mokin, Ondo State, Nigeria
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2014 ). ROS are oxygen averagely reactive species that increase dramatically during periods of environmental stress (ultraviolet ray or heat exposure) and result in significant harm to cell structures ( Dubrovsky 2005 ). Oxidative stress is associated