Oxidative Stress-induced Inhibition of Sirt1 by Caveolin-1 Promotes p53-dependent Premature Senescence and Stimulates the Secretion of Interleukin 6 (IL-6)
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Caveolin 1
Sirtuin 1
Senescence
Reactive nitrogen species
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It is well established that the accumulation of high levels of reactive oxygen species (ROS), due to excessive generation of ROS and/or impaired antioxidant capacity of cells, can result in oxidative stress and cause oxidative damage to cells and their functions [...]
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Atherosclerosis is the commonest cause of death in the world and one of the most important processes that occurs with increasing age because it is accompanied by progressive endothelial dysfunction. Recent studies demonstrated that Sirtuin 1 (SIRT1) might potentially affect cell senescence. However, the effect of SIRT1 on the regulation of human umbilical vein endothelial cell (HUVEC) senescence with total flavonoids (TFs) has not been addressed previously. This study investigated how SIRT1 functions in the process of HUVEC senescence when TFs are present and identified the potential molecular mechanisms involved. Using a model of HUVEC senescence induced by angiotensin II, TFs pretreatment reduced the percentage of senescence-associated β -galactosidase (SA- β -gal) cells and p53 mRNA expression. The level of SIRT1 protein and E2F1 decreased during HUVEC senescence and could be partially recovered when cells were coincubated with TFs, while the levels of proteins p53 and p21 increased during cell senescence and diminished in response to the TFs treatment. When coincubated with 20 mM nicotinamide, the results with SA- β -gal-positive cells and the expression of SIRT1, E2F1, p53, and p21 were contrary to that obtained with only TFs pretreatment. The data indicate that the TFs exert their effect on HUVEC senescence through SIRT1.
Senescence
Sirtuin 1
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The concept and manifestation of stress and forms of environmental stress which was defined as a biological response to an event that an individual perceives as a threat to its homeostasis are linked to the activation of the hypothalamo-pituitary-adrenal system. Under normal conditions, cells have well-developed antioxidants systems that minimize the pertubations caused by reactive oxygen species (ROS). However, when ROS generations are increased to an extent that they overcome the cellular antioxidants then oxidative stress results. Oxidative stress is seen as a battle between inducers (pro-oxidants) and protective factors (antioxidants), because ROS are partially products of oxygen; they have a high chemical reactivity with other bio-macromolecules that may lead to lipid peroxidation and oxidation. Due to this reactivity, oxidative stress is thought to play an important role in the pathogenesis of environmental stress. Keywords : Environmental stress, Reactive oxygen species, Oxidative stress, Antioxidants.
Homeostasis
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Reactive oxygen species (ROS) are the molecular oxygen derivatives that have at least one unpaired electron. Thus, ROS easily react with a number of cell structures causing a change in their functions. ROS produced in small quantities positively affect many cellular mechanisms, but in excess are responsible for the formation of oxidative stress. Oxidative stress is considered a major cause of many diseases, including cardiovascular disease. Abolition of the adverse effects of ROS on organisms in order to maintain redox homeostasis is possible thanks to antioxidants. The research conducted mainly in recent years shows that the formation of arrhythmias may also be related to the phenomenon of oxidative stress. Oxidative damage to cell membranes in particular are causing changes in ion channel activity, which proper functioning is the basis for the formation of normal heart rhythm. Antioxidants seem to play a protective role against the formation of arrhythmias.
Homeostasis
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Oxidative stress is an imbalance between the production of a reactive oxygen species and the antioxidant defense, leading to tissue damage. The produced reactive oxygen species, such as superoxide anion, hydroxyl radical, and peroxyl radical result in damage to many biological molecules (including DNA, lipids, and protein), and the prolonged existence of these reactive oxygen species promotes severe tissue damage and cell death.[1,2] It has been proposed that there is a causal relationship between insulin resistance, oxidative stress, and periodontitis and that hyperglycemia is a major factor responsible for the activation of oxidative stress.[1,2]
Hydroxyl radical
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Mitochondria are known to generate approximately 90% of cellular reactive oxygen species (ROS). The imbalance between mitochondrial reactive oxygen species (mtROS) production and removal due to overproduction of ROS and/or decreased antioxidants defense activity results in oxidative stress (OS), which leads to oxidative damage that affects several cellular components such as lipids, DNA, and proteins. Since the kidney is a highly energetic organ, it is more vulnerable to damage caused by OS and thus its contribution to the development and progression of chronic kidney disease (CKD). This article aims to review the contribution of mtROS and OS to CKD progression and kidney function deterioration.
Mitochondrial ROS
Overproduction
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Senescence is a genetically regulated process that involves decomposition of cellular structures and distribution of the products of this degradation to other plant parts. Reactions involving reactive oxygen species are the intrinsic features of these processes and their role in senescence is suggested. The malfunction of protection against destruction induced by reactive oxygen species could be the starting point of senescence. This article reviews biochemical changes during senescence in relation to reactive oxygen species and changes in antioxidant protection.
Senescence
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