scholarly journals H2S as a Bridge Linking Inflammation, Oxidative Stress and Endothelial Biology: A Possible Defense in the Fight against SARS-CoV-2 Infection?

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1107
Author(s):  
Francesca Gorini ◽  
Serena Del Turco ◽  
Laura Sabatino ◽  
Melania Gaggini ◽  
Cristina Vassalle
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Endothelial Dysfunction ◽  
Vascular Injury ◽  
Biological Functions ◽  
Therapeutic Approaches ◽  
Endothelium Dysfunction ◽  
Physiological Homeostasis ◽  
Vessel Integrity

The endothelium controls vascular homeostasis through a delicate balance between secretion of vasodilators and vasoconstrictors. The loss of physiological homeostasis leads to endothelial dysfunction, for which inflammatory events represent critical determinants. In this context, therapeutic approaches targeting inflammation-related vascular injury may help for the treatment of cardiovascular disease and a multitude of other conditions related to endothelium dysfunction, including COVID-19. In recent years, within the complexity of the inflammatory scenario related to loss of vessel integrity, hydrogen sulfide (H2S) has aroused great interest due to its importance in different signaling pathways at the endothelial level. In this review, we discuss the effects of H2S, a molecule which has been reported to demonstrate anti-inflammatory activity, in addition to many other biological functions related to endothelium and sulfur-drugs as new possible therapeutic options in diseases involving vascular pathobiology, such as in SARS-CoV-2 infection.

scholarly journals Circulating Hydrogen Sulfide (H2S) and Nitric Oxide (NO) Levels Are Significantly Reduced in HIV Patients Concomitant with Increased Oxidative Stress Biomarkers

2021 ◽  
Vol 10 (19) ◽  
pp. 4460
Author(s):  
Rahib K. Islam ◽  
Erinn Donnelly ◽  
Kazi N. Islam
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Normal Subjects ◽  
Plasma Samples ◽  
Hiv Patients ◽  
Hs Crp ◽  
Circulating Levels ◽  
Gaseous Signaling Molecules

Human immunodeficiency virus (HIV) attacks the immune system and weakens the ability to fight infections/disease. Furthermore, HIV infection confers approximately two-fold higher risk of cardiac events compared with the general population. The pathological mechanisms responsible for the increased incidence of cardiovascular disease in HIV patients are largely unknown. We hypothesized that increased oxidative stress and attenuated circulating levels of the cardioprotective gaseous signaling molecules, nitric oxide (NO), and hydrogen sulfide (H2S) were involved in the cardiovascular pathobiology observed in HIV patients. Plasma samples from both HIV patients and age–matched normal subjects were used for all assays. Oxidative stress was determined by analyzing the levels of advanced oxidation protein products (AOPP) and H2O2. Antioxidant levels were determined by measuring the levels of trolox equivalent capacity. ADMA, hs-CRP, and IL-6 were determined by using ELISA. The levels of H2S (free H2S and sulfane sulfur) and NO2 (nitrite) were determined in the plasma samples by using gas chromatography and HPLC, respectively. In the present study we observed a marked induction in the levels of oxidative stress and decreased antioxidant status in the plasma of HIV patients as compared with the controls. Circulating levels of the cardiovascular disease biomarkers: ADMA, hs-CRP (high-sensitivity C-reactive protein), and IL-6 were significantly increased in the circulatory system of HIV patients. The levels of both nitrite and H2S/sulfane sulfur were significantly reduced in the plasma of HIV patients as compared with normal subjects. Our data demonstrate significant increases in circulating biomarkers of oxidative stress and cardiovascular (CV) in conjunction with decreased bioavailability of H2S and NO in HIV patients. Diminished levels of these two cardioprotective gaseous signaling molecules may be involved in the pathogenesis of CV disease in the setting of HIV.

scholarly journals The Benefits of Fasting to Improve Health Conditions and to Prevent Cardiovascular Disease

Jurnal NERS ◽  
2020 ◽  
Vol 14 (3) ◽  
pp. 383
Author(s):  
Wahyu Sukma Samudera ◽  
Gracia Victoria Fernandez ◽  
Rahmatul Fitriyah ◽  
Hidayat Arifin ◽  
Shenda Maulina Wulandari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Cardiovascular Disease ◽  
At Risk ◽  
Body Weight ◽  
Endothelial Dysfunction ◽  
Fasting Blood Glucose ◽  
Abdominal Circumference ◽  
Oxidative Stress Marker ◽  
Amyloid A

Introduction: Fasting is defined as the voluntary abstinence from eating for variable time intervals and it has been associated with potential beneficial impacts on human health. The study was to review the benefits of fasting on cardiovascular health in humans with or without cardiovascular disease.Methods: The databases search was done using the keywords ‘fasting’ and ‘cardiovascular system’ using Scopus, Science Direct and ProQuest, limited to between 2013 and 2019 for publication year. A total of 3.619 articles were obtained and 15 articles involving experimental and non-experimental studies were used as the reference material.Results: The findings showed that in people who are healthy, fasting can reduce the inflammatory markers (IL-1 & IL-6, TNF-α), the oxidative stress marker (Malondialdehyde), body weight, abdominal circumference, fasting blood glucose, LDL, triglyceride and blood pressure. In people at risk or with cardiovascular disease, fasting can reduce body weight, body mass index, abdominal circumference, fat percentage, blood pressure, triglyceride, the biomarker of inflammation (serum amyloid A), the biomarker of oxidative stress (protein carbonyl), the biomarker of endothelial dysfunction (asymmetric dimethylarginine) and increase the vascular endothelial growth factor.Conclusion: Based on these findings, fasting can improve the health condition of people at risk or with cardiovascular disease by improving the risk factors such as blood pressure, overweight and endothelial dysfunction. In people who are healthy, fasting can be used for the prevention of cardiovascular disease by helping to maintain their weight, blood pressure, LDL and triglyceride within the normal limits.

Abstract 14746: Dynamic SIRTUIN1-modulated Lysine Acetylation of P66shc Governs Vascular Endothelial Oxidative Stress and Dysfunction of Diabetes

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Santosh Kumar ◽  
Young Rae Kim ◽  
Ajit Vikram ◽  
Asma Naqvi ◽  
Ajay Kumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Vascular Dysfunction ◽  
Stress Protein ◽  
Lysine Acetylation ◽  
Vascular Endothelial ◽  
Endothelium Dysfunction ◽  
Lysine Deacetylase ◽  
Oxidative Function

The SIRTUIN1 lysine deacetylase (SIRT1) ameliorates diabetic vascular dysfunction by epigenetically suppressing endothelial expression of the oxidative stress protein p66shc. However, whether SIRT1 modulates the oxidative function of p66shc by directly targeting it for lysine deacetylation is not known. Here we show that the oxidative function of p66shc is dynamically modulated by lysine acetylation. Mass spectroscopy identified lysine 81 in the unique CH2 domain of p66shc as the residue targeted by SIRT1. High glucose and SIRT1 knockdown stimulates acetylation of lysine 81 of endothelial p66shc. Compared to WT p66shc, non-acetylatable (K81R) p66shc is significantly handicapped in promoting endothelial hydrogen peroxide production stimulated by high glucose. Compared to WT p66shc, K81R p66shc is also less prone to serine 36 phosphorylation by high glucose, which is essential for the oxidative function of p66shc. Moreover, in contrast to WT p66shc which worsens endothelial dysfunction, expression of K81R p66shc does not impair endothelial function in wild type mice and rescues endothelium dysfunction of diabetic db+/db+ mouse aortas . These findings show that lysine 81 acetylation promotes the oxidative role of p66shc in hyperglycemic conditions, and is essential for p66shc-mediated endothelial dysfunction.

P6266Circulating microparticules of patients with coronary artery disease up-regulate the expression of sodium-glucose cotransporters 1 and 2 in coronary artery endothelial cells: role of angiotensin II

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Park ◽  
E Belcastro ◽  
H Hasan ◽  
C Bruckert ◽  
B Marchandot ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Protein Level ◽  
Immunocytochemical Staining ◽  
Ang Ii ◽  
Angiotensin System

Abstract Introduction Circulating microparticles (MPs) from patients with coronary artery diseases (CAD) have been shown to promote endothelial senescence and dysfunction involving the pro-oxidant local angiotensin system. Sodium-glucose cotransporters (SGLTs)2 inhibitors decreased the risk of cardiovascular disease in patients with type 2 diabetes and this effect appears to be independent of glycemic control. Moreover, high glucose and H2O2 have been shown to cause a redox-sensitive upregulation of SGLT1 and 2 in coronary artery endothelial cells (ECs). Aim Therefore, this study examined whether angiotensin II (Ang II, a potent NADPH oxidase-dependent inducer of oxidative stress) and CAD MPs stimulate SGLT1 and 2 expression in ECs, and assessed their role in the induction of endothelial dysfunction. Methods ECs were isolated from porcine coronary arteries. The protein expression level was assessed by Western blot analysis and immunocytochemical staining, oxidative stress using dihydroethidium staining, and senescence by senescence-associated beta-galactosidase activity (SA-beta-gal activity). Circulating CAD MPs were collected from blood samples of patients (61–79 year) with established cardiovascular disease. Results Control ECs expressed low levels of SGLT1 and SGLT2 proteins. Exposure of ECs to Ang II caused a time- and concentration-dependent increase in the protein level of SGLT1 and SGLT2 with a significant increase observed at concentrations as low as 10 nM. Exposure of ECs to CAD MPs (10 nM PhtdSer eq) from 3/5 patients increased the SGLT1 and SGLT2 protein level. An increased SGLT1 and SGLT2 immunofluorescence signal was also observed in response to Ang II and H2O2. Ang II increased the level of oxidative stress, SA-beta-gal activity, senescence markers (p53, p21 and p16), VCAM-1, MCP-1, tissue factor (TF) and the local angiotensin system (ACE, AT1R), and down-regulated that of eNOS. CAD MPs from 4/5 patients decreased eNOS level and from 5/5 patients increased VCAM-1 level. All the Ang II-induced effects were prevented by the dual SGLT1/2 inhibitor LX-4211 and the selective SGLT2 inhibitor, empagliflozin. Conclusions The present findings indicate that CAD MPs and Ang II upregulate the expression of SGLT1 and SGLT2 protein levels in ECs, and that they promote endothelial dysfunction. They further suggest that inhibition of SGLT1 and/or SGLT2 might be an attractive strategy to protect the arterial wall and, hence, the development of cardiovascular diseases. Acknowledgement/Funding Unrestricted research grant from Boehringer Ingelheim Pharma GmbH & Co. KG

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