scholarly journals Reactive Oxygen Species-Mediated Control of Mitochondrial Biogenesis

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Edgar D. Yoboue ◽  
Anne Devin
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Biogenesis ◽  
Redox State ◽  
Mitochondrial Genomes ◽  
Oxygen Species ◽  
Mitochondrial Content ◽  
Cellular Redox ◽  
High Importance ◽  
Complex Process ◽  
Long Time

Mitochondrial biogenesis is a complex process. It necessitates the contribution of both the nuclear and the mitochondrial genomes and therefore crosstalk between the nucleus and mitochondria. It is now well established that cellular mitochondrial content can vary according to a number of stimuli and physiological states in eukaryotes. The knowledge of the actors and signals regulating the mitochondrial biogenesis is thus of high importance. The cellular redox state has been considered for a long time as a key element in the regulation of various processes. In this paper, we report the involvement of the oxidative stress in the regulation of some actors of mitochondrial biogenesis.

Reactive oxygen species in cell signaling

2000 ◽  
Vol 279 (6) ◽  
pp. L1005-L1028 ◽  
Author(s):  
Victor J. Thannickal ◽  
Barry L. Fanburg
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signal Transduction ◽  
Plasma Membrane ◽  
Growth Factors ◽  
Redox State ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cellular Redox ◽  
By Products

Reactive oxygen species (ROS) are generated as by-products of cellular metabolism, primarily in the mitochondria. When cellular production of ROS overwhelms its antioxidant capacity, damage to cellular macromolecules such as lipids, protein, and DNA may ensue. Such a state of “oxidative stress” is thought to contribute to the pathogenesis of a number of human diseases including those of the lung. Recent studies have also implicated ROS that are generated by specialized plasma membrane oxidases in normal physiological signaling by growth factors and cytokines. In this review, we examine the evidence for ligand-induced generation of ROS, its cellular sources, and the signaling pathways that are activated. Emerging concepts on the mechanisms of signal transduction by ROS that involve alterations in cellular redox state and oxidative modifications of proteins are also discussed.

scholarly journals Use of Exogenous and Endogenous Photomediators as Efficient ROS Modulation Tools: Results and Perspectives for Therapeutic Purposes

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Maria Rosa Antognazza ◽  
Ilaria Abdel Aziz ◽  
Francesco Lodola
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Fluorescent Probes ◽  
State Of The Art ◽  
Polymeric Materials ◽  
Living Systems ◽  
Oxygen Species ◽  
Recent Developments ◽  
Long Time

Reactive Oxygen Species (ROS) play an essential dual role in living systems. Healthy levels of ROS modulate several signaling pathways, but at the same time, when they exceed normal physiological amounts, they work in the opposite direction, playing pivotal functions in the pathophysiology of multiple severe medical conditions (i.e., cancer, diabetes, neurodegenerative and cardiovascular diseases, and aging). Therefore, the research for methods to detect their levels via light-sensitive fluorescent probes has been extensively studied over the years. However, this is not the only link between light and ROS. In fact, the modulation of ROS mediated by light has been exploited already for a long time. In this review, we report the state of the art, as well as recent developments, in the field of photostimulation of oxidative stress, from photobiomodulation (PBM) mediated by naturally expressed light-sensitive proteins to the most recent optogenetic approaches, and finally, we describe the main methods of exogenous stimulation, in particular highlighting the new insights based on optically driven ROS modulation mediated by polymeric materials.

Reassessing cellular glutathione homoeostasis: novel insights revealed by genetically encoded redox probes

2014 ◽  
Vol 42 (4) ◽  
pp. 979-984 ◽  
Author(s):  
Bruce Morgan
Keyword(s):  
Oxidative Stress ◽  
Small Molecule ◽  
Redox State ◽  
Eukaryotic Cell ◽  
Yeast Cells ◽  
Cellular Redox ◽  
Whole Cell ◽  
New Findings ◽  
Cytosolic Glutathione ◽  
Cellular Redox State

Glutathione is the most abundant small molecule thiol in nearly all eukaryotes. Whole-cell levels of oxidized (GSSG) and reduced (GSH) glutathione are variable and responsive to genetic and chemical manipulations, which has led to their relative levels being widely used as a marker of the ‘cellular redox state’ and to indicate the level of ‘oxidative stress’ experienced by cells, tissues and organisms. However, the applicability of glutathione as a marker for a generalized ‘cellular redox state’ is questionable, especially in the light of recent observations in yeast cells. In yeast, whole-cell GSSG changes are almost completely dependent upon the activity of an ABC-C (ATP-binding cassette-C) transporter, Ycf1 (yeast cadmium factor 1), which mediates sequestration of GSSG to the vacuole. In the absence of Ycf1 whole-cell GSSG content is strongly decreased and extremely robust to perturbation. These observations are consistent with highly specific redox-sensitive GFP probe-based measurements of the cytosolic glutathione pool and indicate that cytosolic GSSG reductive systems are easily able to reduce nearly all GSSG formed, even following treatment with large concentrations of oxidant. In the present paper, I discuss the consequences of these new findings for our understanding of glutathione homoeostasis in the eukaryotic cell.

scholarly journals Spirulina-PCL Nanofiber Wound Dressing to Improve Cutaneous Wound Healing by Enhancing Antioxidative Mechanism

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Sang-Myung Jung ◽  
Seul Ki Min ◽  
Hoo Chul Lee ◽  
Yeo Seon Kwon ◽  
Moon Hee Jung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wound Dressing ◽  
Skin Regeneration ◽  
Oxygen Species ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Blue Green Algae ◽  
Antioxidant Mechanism ◽  
Complex Process

Skin regeneration is a complex process involving massive proliferation and alignment of cells, where there are obstacles to completion of regeneration, the main one being excessive generation of reactive oxygen species (ROS) from inflammation or infection.Spirulina, blue-green algae that has antioxidant and anti-inflammatory activities, has been used to relieve such ROS stress. In this study,Spirulinaextract loaded PCL (Spirulina-PCL) nanofiber was evaluated as a cutaneous wound dressing in view of antioxidative mechanism. In addition to increasing fibroblast viability, theSpirulinaextract and its dressing modulated intra- and extracellular ROS by enhancing antioxidant mechanism of fibroblast under oxidative stress. Finally,in vivoassays confirmed thatSpirulina-PCL helps regenerate wounds and enhance regeneration. Taken together, the results of this study indicate thatSpirulinaand nanofiber have the potential for application to cutaneous wound to facilitate skin regeneration.

scholarly journals Oxidative Stress and ROS-Mediated Signaling in Leukemia: Novel Promising Perspectives to Eradicate Chemoresistant Cells in Myeloid Leukemia

2021 ◽  
Vol 22 (5) ◽  
pp. 2470
Author(s):  
Silvia Trombetti ◽  
Elena Cesaro ◽  
Rosa Catapano ◽  
Raffaele Sessa ◽  
Alessandra Lo Bianco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myeloid Leukemia ◽  
Molecular Mechanisms ◽  
Hematological Malignancies ◽  
Leukemic Cells ◽  
Leukemia Cells ◽  
Ros Production ◽  
Oxygen Species ◽  
Cellular Redox ◽  
Ros Homeostasis

Myeloid leukemic cells are intrinsically under oxidative stress due to impaired reactive oxygen species (ROS) homeostasis, a common signature of several hematological malignancies. The present review focuses on the molecular mechanisms of aberrant ROS production in myeloid leukemia cells as well as on the redox-dependent signaling pathways involved in the leukemogenic process. Finally, the relevance of new chemotherapy options that specifically exert their pharmacological activity by altering the cellular redox imbalance will be discussed as an effective strategy to eradicate chemoresistant cells.

scholarly journals The Mitochondria: A Target of Polyphenols in the Treatment of Diabetic Cardiomyopathy

2020 ◽  
Vol 21 (14) ◽  
pp. 4962 ◽  
Author(s):  
Humna Bhagani ◽  
Suzanne A. Nasser ◽  
Ali Dakroub ◽  
Ahmed F. El-Yazbi ◽  
Assaad A. Eid ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Glucose Metabolism ◽  
Protective Effect ◽  
Diabetic Cardiomyopathy ◽  
Mitochondrial Biogenesis ◽  
Ventricular Dysfunction ◽  
Therapeutic Targets ◽  
Ros Production ◽  
Oxygen Species

Diabetic cardiomyopathy (DCM) is a constellation of symptoms consisting of ventricular dysfunction and cardiomyocyte disarray in the presence of diabetes. The exact cause of this type of cardiomyopathy is still unknown; however, several processes involving the mitochondria, such as lipid and glucose metabolism, reactive oxygen species (ROS) production, apoptosis, autophagy and mitochondrial biogenesis have been implicated. In addition, polyphenols have been shown to improve the progression of diabetes. In this review, we discuss some of the mechanisms by which polyphenols, particularly resveratrol, play a role in slowing the progression of DCM. The most important intermediates by which polyphenols exert their protective effect include Bcl-2, UCP2, SIRT-1, AMPK and JNK1. Bcl-2 acts to attenuate apoptosis, UCP2 decreases oxidative stress, SIRT-1 increases mitochondrial biogenesis and decreases oxidative stress, AMPK increases autophagy, and JNK1 decreases apoptosis and increases autophagy. Our dissection of these molecular players aims to provide potential therapeutic targets for the treatment of DCM.

scholarly journals Rgs12 enhances osteoclastogenesis by suppressing Nrf2 activity and promoting the formation of reactive oxygen species

2018 ◽  
Author(s):  
Andrew YH Ng ◽  
Ziqing Li ◽  
Megan M Jones ◽  
Chengjian Tu ◽  
Merry J Oursler ◽  
...  
Keyword(s):  
Redox State ◽  
26S Proteasome ◽  
G Protein Signaling ◽  
Oxygen Species ◽  
Protein Signaling ◽  
Antioxidant Treatment ◽  
Proteomics Analysis ◽  
Cellular Redox

ABSTRACTThe Regulator of G-protein Signaling 12 (Rgs12) is important for osteoclast (OC) differentiation, and its deletion in vivo protected mice against pathological bone loss. To characterize its mechanism in osteoclastogenesis, we selectively deleted Rgs12 in OC precursors using the LysM-Cre transgenic line or overexpressed the gene in RAW264.7 cells. Rgs12 deletion led to increased bone mass with decreased OC numbers, whereas its overexpression increased OC number and size. Proteomics analysis of Rgs12-deficient OCs identified an upregulation of antioxidant enzymes under the transcriptional regulation of Nrf2, the master regulator of oxidative stress. We confirmed an increase of Nrf2 activity and impaired production in Rgs12-deficient cells. Conversely, Rgs12 overexpression suppressed Nrf2 through a mechanism dependent on the 26S proteasome, and promoted RANKL-induced phosphorylation of ERK1/2 and NFκB, which was abrogated by antioxidant treatment. We therefore identified a novel role of Rgs12 in regulating Nrf2, thereby controlling cellular redox state and OC differentiation.

scholarly journals Scarred Lung. An Update on Radiation-Induced Pulmonary Fibrosis

2021 ◽  
Vol 7 ◽  
Author(s):  
Natalia Jarzebska ◽  
Ekaterina S. Karetnikova ◽  
Alexander G. Markov ◽  
Michael Kasper ◽  
Roman N. Rodionov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Fibrosis ◽  
Lung Fibrosis ◽  
Treatment Options ◽  
Inflammatory Cells ◽  
Oxygen Species ◽  
Current State ◽  
Complex Process ◽  
Long Time ◽  
Radiation Induced

Radiation-induced pulmonary fibrosis is a common severe long-time complication of radiation therapy for tumors of the thorax. Current therapeutic options used in the clinic include only supportive managements strategies, such as anti-inflammatory treatment using steroids, their efficacy, however, is far from being satisfactory. Recent studies have demonstrated that the development of lung fibrosis is a dynamic and complex process, involving the release of reactive oxygen species, activation of Toll-like receptors, recruitment of inflammatory cells, excessive production of nitric oxide and production of collagen by activated myofibroblasts. In this review we summarized the current state of knowledge on the pathophysiological processes leading to the development of lung fibrosis and we also discussed the possible treatment options.

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