scholarly journals Antioxidant enzymes and vascular diseases

2021 ◽  
pp. 544-555
Author(s):  
Jelena Radovanovic ◽  
Katarina Banjac ◽  
Milan Obradovic ◽  
Esma R. Isenovic
Keyword(s):  
Antioxidative Enzymes ◽  
Reactive Nitrogen Species ◽  
Antioxidant Defense ◽  
Vascular System ◽  
Vascular Diseases ◽  
Mitochondrial Respiratory Chain ◽  
Vascular Endothelial ◽  
Physiological Conditions ◽  
Oxidative Balance ◽  
Redox Active

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play a fundamental role in regulating endothelial function and vascular tone in the physiological conditions of a vascular system. However, oxidative stress has detrimental effects on human health, and numerous studies confirmed that high ROS/RNS production contributes to the initiation and progression of cardiovascular diseases. The antioxidant defense has an essential role in the homeostatic functioning of the vascular endothelial system. Endogenous antioxidative defense includes various molecules and enzymes such as superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase. Together all these antioxidative enzymes are essential for defense against harmful ROS features. ROS are mainly generated from redox-active compounds involved in the mitochondrial respiratory chain. Thus, targeting antioxidative enzymes and mitochondria oxidative balance may be a promising approach for vascular diseases occurrence and treatment. This review summarized the most recent research on the regulation of antioxidative enzymes in vascular diseases.

scholarly journals Exogenous ascorbic acid is a pro-nitrant in Arabidopsis thaliana

2019 ◽  
Vol 62 (2) ◽  
pp. 115-122
Author(s):  
Gábor Feigl ◽  
Ádám Bordé ◽  
Árpád Molnár ◽  
Zsuzsanna Kolbert
Keyword(s):  
Ascorbic Acid ◽  
Reactive Nitrogen Species ◽  
Redox State ◽  
Plant Biology ◽  
Wild Type ◽  
Physiological Conditions ◽  
Redox Active ◽  
Tight Correlation ◽  
Mutant Lines ◽  
First Time

Due to the intensified production of reactive nitrogen species (RNS) proteins can be modified by tyrosine nitration (PTN). Examination of PTN is a hot topic of plant biology, especially because the exact outcome of this modification is still pending. Both RNS and ascorbic acid (AsA) are redox-active molecules, which directly affect the redox state of cells. The possible link between RNS-dependent PTN and AsA metabolism was studied in RNS (gsnor1-3, nia1nia2) and AsA (vtc2-3) homeostasis Arabidopsis mutants. During physiological conditions, intensified PTN was detected in all mutant lines compared to the wild-type (WT); without altering nitration pattern. Moreover, the increased PTN seemed to be associated with endogenous peroxynitrite (ONOO-) levels, but it showed no tight correlation with endogenous levels of nitric-oxide (NO) or AsA. Exogenous AsA caused intensified PTN in WT, vtc2-3 and nia1nia2. In the background of increased PTN, significant NO and ONOO- accumulation was detected, indicating exogenous AsA-induced RNS burst. Interestingly, in AsA-triggered stress-situation, changes of NO levels seem to be primarily connected to the development of PTN. Our results point out for the first time that similarly to human and animal systems exogenous AsA exerts pro-nitrant effect on plant proteome.

scholarly journals Role of NFAT in the Progression of Diabetic Atherosclerosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Yaoyao Cai ◽  
Haipeng Yao ◽  
Zhen Sun ◽  
Ying Wang ◽  
Yunyun Zhao ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cardiovascular System ◽  
Signaling Pathways ◽  
Immune Cells ◽  
Target Genes ◽  
Vascular System ◽  
Foam Cell ◽  
Vascular Diseases ◽  
Regulatory Function ◽  
Foam Cell Formation

Nuclear factor of activated T cells (NFAT) is a transcription factor with a multidirectional regulatory function, that is widely expressed in immune cells, including cells in the cardiovascular system, and non-immune cells. A large number of studies have confirmed that calcineurin/NFAT signal transduction is very important in the development of vascular system and cardiovascular system during embryonic development, and plays some role in the occurrence of vascular diseases such as atherosclerosis, vascular calcification, and hypertension. Recent in vitro and in vivo studies have shown that NFAT proteins and their activation in the nucleus and binding to DNA-related sites can easily ɨnduce the expression of downstream target genes that participate in the proliferation, migration, angiogenesis, and vascular inflammation of vascular wall related cells in various pathophysiological states. NFAT expression is regulated by various signaling pathways, including CD137-CD137L, and OX40-OX40L pathways. As a functionally diverse transcription factor, NFAT interacts with a large number of signaling molecules to modulate intracellular and extracellular signaling pathways. These NFAT-centered signaling pathways play important regulatory roles in the progression of atherosclerosis, such as in vascular smooth muscle cell phenotypic transition and migration, endothelial cell injury, macrophage-derived foam cell formation, and plaque calcification. NFAT and related signaling pathways provide new therapeutic targets for vascular diseases such as atherosclerosis. Hence, further studies of the mechanism of NFAT in the occurrence and evolution of atherosclerosis remain crucial.

Abstract 476: Attenuated Activities of Mitochondria in Vascular Endothelial Cells Exposed to Oxidized or Glycated Low Density Lipoprotein

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Garry X Shen ◽  
Subir K Roy Chowdhury
Keyword(s):  
Endothelial Cells ◽  
Respiratory Chain ◽  
Complex I ◽  
Vascular Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Mitochondrial Respiratory Chain ◽  
Low Density ◽  
Vascular Endothelial ◽  
Glycated Ldl

Hyperglycemia and dyslipoproteinemia are two major biochemical markers of diabetes. Elevated low density lipoprotein (LDL) is a classical risk factor for atherosclerotic cardiovascular disease. Our previous studies demonstrated that oxidized LDL (ox-LDL) and glycated LDL (gly-LDL) increased the generation of reactive oxygen species (ROS) in vascular endothelial cells. ROS is implicated in endothelial dysfunction and diabetic vascular complications. Mitochondria are an important source of ROS in the body. We hypothesize that ox-LDL or gly-LDL might affect the activity of mitochondrial respiratory chain. We evaluated the activities of mitochondrial respiratory chain complexes in porcine aortic endothelial cells (PAEC) using OROBORS oxygraph. The oxygraph was used as a highly sensitive tool to evaluate mitochondrial complex activity in freshly harvested and digitonin-permeabilized PAEC (for Complex I, the rotenone-sensitive oxidation of glutamate + malate in the presence of ADP; Complex II, antimycin A-sensitive oxidation of succinate; Complex IV, potassium cyanide-sensitive oxidation of ascorbate + TMPD). The oxygen consumption in Complex I, II and IV of PAEC was significantly decreased by >12 h of incubation with LDL, ox-LDL or gly-LDL compared to control cultures. Attenuated activity of succinate cytochrome C reductase was detected in EC treated with LDL, ox-LDL or gly-LDL for 24 h. Decreased levels of respiratory control ratio were detected in EC treated with LDL or ox-LDL for 6 h, but not for 2 h, compared to control. Impaired activity of mitochondrial complexes can cause electron leakage in the respiratory chain and substantially increase ROS formation. The findings suggest that oxidized or glycated LDL attenuates mitochondrial activities in vascular EC, which may contribute to increased ROS generation and endothelial dysfunction induced by the atherogenic lipoproteins (supported by operating grants from Canadian Institute of Health Research and Canadian Diabetes Association).

Nitric oxide and regulation of vascular tone: pharmacological and physiological considerations

1998 ◽  
Vol 7 (2) ◽  
pp. 131-140 ◽  
Author(s):  
J McHugh ◽  
DJ Cheek
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular System ◽  
Biological Activities ◽  
Vascular Diseases ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Physical Stimuli ◽  
Artery Disease

The endothelial cells of the vascular system are responsible for many biological activities that maintain vascular homeostasis. Responding to a variety of chemical and physical stimuli, the endothelium elaborates a host of vasoactive agents. One of these agents, endothelium-derived relaxing factor, now accepted as nitric oxide, influences both cellular constituents of the blood and vascular smooth muscle. A principal intracellular target for nitric oxide is guanylate cyclase, which, when activated, increases the intracellular concentration of cyclic guanosine monophosphate, which in turn activates protein kinase G. Acting by this pathway, nitric oxide induces relaxation of vascular smooth muscle and inhibits platelet activation and aggregation. Derangements in endothelial production of nitric oxide are implicated as both cause and consequence of vascular diseases, including hypertension, atherosclerosis, and coronary artery disease.

scholarly journals Therapies for Neovascular Age-Related Macular Degeneration: Current Approaches and Pharmacologic Agents in Development

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Mostafa Hanout ◽  
Daniel Ferraz ◽  
Mehreen Ansari ◽  
Natasha Maqsood ◽  
Saleema Kherani ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Vascular Diseases ◽  
Age Related Macular Degeneration ◽  
Treatment Modalities ◽  
Vascular Endothelial ◽  
New Therapies ◽  
Age Related ◽  
Early Phase Clinical Trials ◽  
Endothelial Growth Factor ◽  
Pharmacologic Agents

As one of the leading causes of blindness, age-related macular degeneration (AMD) has remained at the epicenter of clinical research in ophthalmology. During the past decade, focus of researchers has ranged from understanding the role of vascular endothelial growth factor (VEGF) in the angiogenic cascades to developing new therapies for retinal vascular diseases. Anti-VEGF agents such as ranibizumab and aflibercept are becoming increasingly well-established therapies and have replaced earlier approaches such as laser photocoagulation or photodynamic therapy. Many other new therapeutic agents, which are in the early phase clinical trials, have shown promising results. The purpose of this paper is to briefly review the available treatment modalities for neovascular AMD and then focus on promising new therapies that are currently in various stages of development.

scholarly journals Genistein Attenuates Vascular Endothelial Impairment in Ovariectomized Hyperhomocysteinemic Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Panpan Zhen ◽  
Qian Zhao ◽  
Dandan Hou ◽  
Teng Liu ◽  
Dongqiao Jiang ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Wistar Rats ◽  
Morphological Changes ◽  
Vascular Diseases ◽  
Bioactive Compound ◽  
Ovariectomized Rats ◽  
Vascular Endothelial ◽  
Female Wistar Rats ◽  
Endothelial Impairment

Hyperhomocysteinemia (HHcy) is a well-known independent risk factor for vascular diseases in the general population. This study was to explore the effect of genistein (GST), a natural bioactive compound derived from legumes, on HHcy-induced vascular endothelial impairment in ovariectomized ratsin vivo. Thirty-two adult female Wistar rats were assigned randomly into four groups (n=8): (a) Con: control; (b) Met: 2.5% methionine diet; (c) OVX + Met: ovariectomy + 2.5% methionine diet; (d) OVX + Met + GST: ovariectomy + 2.5% methionine diet + supplementation with genistein. After 12 wk of different treatment, the rats' blood, toracic aortas and liver samples were collected for analysis. Results showed that high-methionine diet induced both elevation of plasma Hcy and endothelial dysfunction, and ovariectomy deteriorated these injuries. Significant improvement of both functional and morphological changes of vascular endothelium was observed in OVX + Met + GST group; meanwhile the plasma Hcy levels decreased remarkably. There were significant elevations of plasma ET-1 and liver MDA levels in ovariectomized HHcy rats, and supplementation with genistein could attenuate these changes. These results implied that genistein could lower the elevated Hcy levels, and prevent the development of endothelial impairment in ovariectomized HHcy rats. This finding may shed a novel light on the anti-atherogenic activities of genistein in HHcy patients.

Airway epithelium and bronchial reactivity

1987 ◽  
Vol 65 (3) ◽  
pp. 448-450 ◽  
Author(s):  
P. M. Vanhoutte
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelium ◽  
Vessel Wall ◽  
Vascular System ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Blood Vessel Wall ◽  
Respiratory Epithelial Cells ◽  
Relaxing Factor ◽  
Respiratory Epithelial

Damage to or dysfunction of respiratory epithelial cells may contribute to the etiology of bronchial hyperreactivity in asthma and airway infection. In the vascular system, endogenous neurohumoral mediators can cause either relaxation or contraction of the smooth muscle of the blood vessel wall because they cause the release of relaxing or contracting factor(s), respectively, from the vascular endothelial cells. This brief overview summarizes data from the author's laboratory, which suggests that release of relaxing factor(s) from epithelial cells contributes to the regulation of bronchomotor tone.

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