Noncoding RNAs in the Vascular System Response to Oxidative Stress

2019 ◽  
Vol 30 (7) ◽  
pp. 992-1010 ◽  
Author(s):  
Paola Fuschi ◽  
Biagina Maimone ◽  
Carlo Gaetano ◽  
Fabio Martelli
Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 755
Author(s):  
Yoana Rabanal-Ruiz ◽  
Emilio Llanos-González ◽  
Francisco J. Alcain

CoQ10 is an endogenous antioxidant produced in all cells that plays an essential role in energy metabolism and antioxidant protection. CoQ10 distribution is not uniform among different organs, and the highest concentration is observed in the heart, though its levels decrease with age. Advanced age is the major risk factor for cardiovascular disease and endothelial dysfunction triggered by oxidative stress that impairs mitochondrial bioenergetic and reduces NO bioavailability, thus affecting vasodilatation. The rationale of the use of CoQ10 in cardiovascular diseases is that the loss of contractile function due to an energy depletion status in the mitochondria and reduced levels of NO for vasodilatation has been associated with low endogenous CoQ10 levels. Clinical evidence shows that CoQ10 supplementation for prolonged periods is safe, well-tolerated and significantly increases the concentration of CoQ10 in plasma up to 3–5 µg/mL. CoQ10 supplementation reduces oxidative stress and mortality from cardiovascular causes and improves clinical outcome in patients undergoing coronary artery bypass graft surgery, prevents the accumulation of oxLDL in arteries, decreases vascular stiffness and hypertension, improves endothelial dysfunction by reducing the source of ROS in the vascular system and increases the NO levels for vasodilation.


2021 ◽  
Vol 6 (1) ◽  
pp. 179-181
Author(s):  
Rusdiana ◽  
Muhammad Syahputra ◽  
Sry Suryani

Preliminary : Endothelial cells are a single layer that lines the entire vascular system. Endothelial dysfunction can be triggered by several main things, namely physical stress, oxidative stress and irritant substances. Obesity triggers an inflammatory process and metabolic disorders that will lead to increased oxidative stress. Long-term oxidative stress will cause damage to cells and tissues and trigger degenerative diseases. Damage to endothelial cells is expected to be detected by examining Von Willenbrand levels so that it can prevent complications of vascular disorders early. Method: This research is descriptive with cross sectional design. Carried out from March to October 2018 on the USU Campus. The first examination was done to measure body weight and height to determine body mass index, then performed lipid profile and blood sugar levels (KGD) in the sample, then examined von Willenbrand factor levels carried out in the integrated laboratory of USU FK using the method ELISA in both the sample group and the control group. The research subjects were adolescents aged 17-25 years with BMI> 25 kg / m2Data analysis was carried out using the T-Test statistical program, comparing two groups. Result: Of the 40 obese subjects found Von Wilenbrand level values ​​The lowest factor was 1.78 IU / ml and the highest was 35.60 IU / ml. Whereas in 40 non-obese subjects Von Wilenbrand grade values ​​were the lowest factor of 2.01 IU / ml and the highest was 45.10 IU / ml. This difference was not statistically significant (p = 0.661).Conclusion: There was no significant difference between the levels of Von Wilenbrand Factors in obese subjects with non-obese subjectsKey Words: Obesity, endothelial cells, Von Wilenbrand Factors


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e8121 ◽  
Author(s):  
Mingxuan Wang ◽  
Yajuan Zheng

Glaucoma is an age-dependent disease closely related to oxidative stress and is regarded as the second leading cause of irreversible blindness worldwide. In recent years, many studies have shown that morphological and functional abnormalities of the trabecular meshwork (TM) are closely related to glaucoma, especially with respect to oxidative stress. In this review, the mechanisms of oxidative stress in the TM and treatment strategies for this condition, including strategies involving antioxidants, noncoding RNAs and exogenous compounds, are discussed. Although many questions remain to be answered, the reviewed findings provide insights for further research on oxidative stress alleviation in glaucoma and suggest new targets for glaucoma prevention.


2020 ◽  
Vol 33 (17) ◽  
pp. 1209-1229 ◽  
Author(s):  
Leonard Clinton D'Souza ◽  
Shruti Mishra ◽  
Anirban Chakraborty ◽  
Anusmita Shekher ◽  
Anurag Sharma ◽  
...  

2012 ◽  
Vol 303 (3) ◽  
pp. F339-F349 ◽  
Author(s):  
Yoshifuru Tamura ◽  
Katsuyuki Tanabe ◽  
Wataru Kitagawa ◽  
Shunya Uchida ◽  
George F. Schreiner ◽  
...  

Nicorandil exhibits a protective effect in the vascular system, which is thought to be due to vasodilatation from opening ATP-dependent potassium channels and donation of nitric oxide. Recently, nicorandil was shown to be renoprotective in models of acute kidney injury and glomerulonephritis. However, the specific mechanisms of renoprotection are unclear. We evaluated the effect of nicorandil on the rat remnant kidney model of chronic kidney disease. Blood pressure was unchanged by a 10-wk course of nicorandil, while albuminuria was significantly reduced. Glomerular injury and tubulointerstitial injury were also ameliorated by nicorandil. Oxidative stress, as noted by renal nitrotyrosine level and urine 8-hydroxy-2′-deoxyguanosine, were elevated in this model and was significantly reduced by nicorandil treatment. Treatment was associated with maintenance of the mitochondrial antioxidant, manganese SOD, in podocytes and with suppression of xanthine oxidase expression in infiltrating macrophages. Interestingly, these two cell types express sulfonylurea receptor 2 (SUR2), a binding site of nicorandil in the ATP-dependent K channel. Consistently, we found that stimulating SUR2 with nicorandil prevented angiotensin II-mediated upregulation of xanthine oxidase in the cultured macrophage, while xanthine oxidase expression was rather induced by blocking SUR2 with glibenclamide. In conclusion, nicorandil reduces albuminuria and ameliorates renal injury by blocking oxidative stress in chronic kidney disease.


2019 ◽  
Vol 69 (12) ◽  
pp. 3634-3637
Author(s):  
Aurel Nechita ◽  
Ciprian Dinu ◽  
Alexandru Bogdan Ciubara ◽  
Gheorghe Raftu ◽  
Codrina Ancuta

Free radicals are widely recognized as overloaded atoms, molecules or compounds that become unstable when lacking an electron;they steal an electron from various macromolecules (e.g. DNA, RNA, proteins) to chemically stabilize, while preferred targets remains polyunsaturated fatty acids in their membranes. When electron theft produces a chain reaction, normal cell processes turn into a real chaos that ultimately degrades the normal functioning of the cell. Variance of free radicals existing or formed in nature as a result of many processes (ultraviolet radiation, gamma, action specific particles, etc.) makes extremely difficult their classification. A partof the oxygen molecules (O2) that have entered the body through breathing is divided and oxygen atoms become reactive (free radicals) damaging the cell wall by oxidation. Oxidative stress, a term widely used to characterise inflammatory disorders caused by destructive oxygen molecules called free radicals, may exacerbate inflammation and impair immune system response due to free radicals. Oxidative stress is defined as the imbalance between oxidants and antioxidants, in favour of oxidants, with destructive and pathogenic potential. Depending on intensity, oxidative stress can occur inside or outside the cell. Intracellular stress can lead to cell necrosis or a more or less marked disruption of the cell, and may be catastrophic in the case of a non-reproducible cell; the extracellular oxidative stress is cytotoxic. Although considered in the pathobiology of several inflammatory immune-mediated rheumatic conditions, the exact role of oxidative stress in ankylosing spondylitis is still debatable.


2022 ◽  
Vol 2022 ◽  
pp. 1-20
Author(s):  
Yue Ren ◽  
Yanan Liu ◽  
Kaiyang Liu ◽  
Xiaoqian Huo ◽  
Chaoqun Liu ◽  
...  

The pathogenesis of diabetic retinopathy (DR) is complicated, and there is no effective drug. Oxidative stress-induced human retinal microvascular endothelial cells (HRMECs) injury is one of the pathogenic factors for DR. Molecular switches are considered high-risk targets in disease progression. Identification of molecular switch is crucial to interpret the pathogenesis of disease and screen effective ingredients. In this study, a systematic process was executed to discover therapeutic candidates for DR based on HRMECs injury. First of all, the molecular mechanism of HRMECs oxidative stress injury was revealed by transcriptomics and network pharmacology. We found that oxidative stress was one of the pivotal pathogenic factors, which interfered with vascular system development, inflammation, cell adhesion, and cytoskeleton damaged HRMECs through crosstalk. Then, network topology analysis was used to recognize molecular switches. The results indicated that the Keap1-Nrf2-ARE signaling pathway was the molecular switch in HRMECs oxidative stress injury. On this basis, the HEK293-ARE overexpression cell line was applied to obtain 18 active traditional Chinese medicine (TCM) ingredients. Furthermore, andrographolide, one of the 18 candidates, was applied in the HRMECs oxidative stress model to evaluate the accuracy of the systematic process. The efficacy evaluation results showed that andrographolide could regulate oxidative stress, vascular system development, inflammation, adhesion, and skeleton tissue to inhibit HRMECs injury cooperatively. And its mechanism was related to the Nrf2 signaling pathway. Overall, our data suggest that the Nrf2 signaling pathway is the molecular switch in the HRMECs oxidative stress injury. 18 potential Nrf2 agonists are likely to be promising DR candidates.


2021 ◽  
Vol 11 (6) ◽  
pp. 424-432
Author(s):  
K. A. Aitbaev ◽  
I. T. Murkamilov ◽  
Zh. A. Murkamilova ◽  
I. O. Kudaibergenova ◽  
F. A. Yusupov

Oxidative stress is a common sign of aging and cardiovascular disease (CVD), including atherosclerosis, heart failure, hypertension, diabetes mellitus and other diseases of the vascular system. In this regard, in recent years, researchers have shown increased interest in sirtuins (SIRTs) — stress adapters and epigenetic enzymes involved in cellular mechanisms for controlling age-related pathologies, cancer and CVD. Among sirtuins, of which there are seven in mammals (SIRT1-SIRT7), SIRT1 and SIRT6 possess the most cardioprotective, anti-inflammatory, atheroprotective and anti-aging properties. In this review, we present a comprehensive analysis of the latest developments in the field of cellular and molecular signaling pathways controlled by two post-translational modifiers — SIRT1 and SIRT6, which have proven their worth as tools to reduce inflammation and oxidative stress at the level of the cardiovascular system. A deeper understanding of the epigenetic mechanisms through which SIRT1 and SIRT6 exert their cardioprotective effect will have widespread implications and will accelerate the development of selective and effective pharmacological agents for modulating sirtuins for the prevention and treatment of CVD.


Plant Methods ◽  
2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Li Ren ◽  
Shan Deng ◽  
Yunxia Chu ◽  
Yiying Zhang ◽  
Hong Zhao ◽  
...  

Abstract Background Cryopreservation is the best way for long-term in vitro preservation of plant germplasm resources. The preliminary studies found that reactive oxygen species (ROS) induced oxidative stress and ice-induced membrane damage are the fundamental causes of cell death in cryopreserved samples. How to improve plant cryopreservation survival rate is an important scientific issue in the cryobiology field. Results This study found that the survival rate was significantly improved by adding single-wall carbon nanotubes (SWCNTs) to plant vitrification solution (PVS) in cryopreservation of Agapanthus praecox embryogenic callus (EC), and analyzed the oxidative response of cells during the control and SWCNTs-added cryopreservation protocol. The SWCNTs entered EC at the step of dehydration and mainly located around the cell wall and in the vesicles, and most of SWCNTs moved out of EC during the dilution step. Combination with physiological index and gene quantitative expression results, SWCNTs affect the ROS signal transduction and antioxidant system response during plant cryopreservation. The EC treated by SWCNTs had higher antioxidant levels, like POD, CAT, and GSH than the control group EC. The EC mainly depended on the AsA-GSH and GPX cycle to scavenge H2O2 in the control cryopreservation, but depended on CAT in the SWCNTs-added cryopreservation which lead to low levels of H2O2 and MDA. The elevated antioxidant level in dehydration by adding SWCNTs enhanced cells resistance to injury during cryopreservation. The ROS signals of EC were balanced and stable in the SWCNTs-added cryopreservation. Conclusions The SWCNTs regulated oxidative stress responses of EC during the process and controlled oxidative damages by the maintenance of ROS homeostasis to achieve a high survival rate after cryopreservation. This study is the first to systematically describe the role of carbon nanomaterial in the regulation of plant oxidative stress response, and provided a novel insight into the application of nanomaterials in the field of cryobiology.


Author(s):  
Pei-Feng Liu ◽  
Ammad Ahmad Farooqi ◽  
Sheng-Yao Peng ◽  
Tzu-Jung Yu ◽  
Hans-Uwe Dahms ◽  
...  

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