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Mr. Marin Kuntic
Department of Cardiology, Cardiology I, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131 Mainz, Germany

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0 Electronic Cigarette
0 Oxidative Stress
0 Environmental risk factors and their impact on cardiovascular health with a focus on air pollution
0 Cigarette and shisha smoking research
0 Animal models of environmental pollution exposure

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Oxidative Stress
Animal models of environmental pollution exposure

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Journal article
Published: 02 August 2021 in Antioxidants
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Angiotensin II (Ang II) has been implicated in the pathophysiology of various age-dependent ocular diseases. The purpose of this study was to test the hypothesis that Ang II induces endothelial dysfunction in mouse ophthalmic arteries and to identify the underlying mechanisms. Ophthalmic arteries were exposed to Ang II in vivo and in vitro to determine vascular function by video microscopy. Moreover, the formation of reactive oxygen species (ROS) was quantified and the expression of prooxidant redox genes and proteins was determined. The endothelium-dependent artery responses were blunted after both in vivo and in vitro exposure to Ang II. The Ang II type 1 receptor (AT1R) blocker, candesartan, and the ROS scavenger, Tiron, prevented Ang II-induced endothelial dysfunction. ROS levels and NOX2 expression were increased following Ang II incubation. Remarkably, Ang II failed to induce endothelial dysfunction in ophthalmic arteries from NOX2-deficient mice. Following Ang II incubation, endothelium-dependent vasodilation was mainly mediated by cytochrome P450 oxygenase (CYP450) metabolites, while the contribution of nitric oxide synthase (NOS) and 12/15-lipoxygenase (12/15-LOX) pathways became negligible. These findings provide evidence that Ang II induces endothelial dysfunction in mouse ophthalmic arteries via AT1R activation and NOX2-dependent ROS formation. From a clinical point of view, the blockade of AT1R signaling and/or NOX2 may be helpful to retain or restore endothelial function in ocular blood vessels in certain ocular diseases.

ACS Style

Michael Birk; Ewa Baum; Jenia Kouchek Zadeh; Caroline Manicam; Norbert Pfeiffer; Andreas Patzak; Johanna Helmstädter; Sebastian Steven; Marin Kuntic; Andreas Daiber; Adrian Gericke. Angiotensin II Induces Oxidative Stress and Endothelial Dysfunction in Mouse Ophthalmic Arteries via Involvement of AT1 Receptors and NOX2. Antioxidants 2021, 10, 1238 .

AMA Style

Michael Birk, Ewa Baum, Jenia Kouchek Zadeh, Caroline Manicam, Norbert Pfeiffer, Andreas Patzak, Johanna Helmstädter, Sebastian Steven, Marin Kuntic, Andreas Daiber, Adrian Gericke. Angiotensin II Induces Oxidative Stress and Endothelial Dysfunction in Mouse Ophthalmic Arteries via Involvement of AT1 Receptors and NOX2. Antioxidants. 2021; 10 (8):1238.

Chicago/Turabian Style

Michael Birk; Ewa Baum; Jenia Kouchek Zadeh; Caroline Manicam; Norbert Pfeiffer; Andreas Patzak; Johanna Helmstädter; Sebastian Steven; Marin Kuntic; Andreas Daiber; Adrian Gericke. 2021. "Angiotensin II Induces Oxidative Stress and Endothelial Dysfunction in Mouse Ophthalmic Arteries via Involvement of AT1 Receptors and NOX2." Antioxidants 10, no. 8: 1238.

Journal article
Published: 08 July 2021 in Redox Biology
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Epidemiological studies showed that traffic noise has a dose-dependent association with increased cardiovascular morbidity and mortality. Whether microvascular dysfunction contributes significantly to the cardiovascular health effects by noise exposure remains to be established. The connection of inflammation and immune cell interaction with microvascular damage and functional impairment is also not well characterized. Male C57BL/6J mice or gp91phox−/y mice with genetic deletion of the phagocytic NADPH oxidase catalytic subunit (gp91phox or NOX-2) were used at the age of 8 weeks, randomly instrumented with dorsal skinfold chambers and exposed or not exposed to aircraft noise for 4 days. Proteomic analysis (using mass spectrometry) revealed a pro-inflammatory phenotype induced by noise exposure that was less pronounced in noise-exposed gp91phox−/y mice. Using in vivo fluorescence microscopy, we found a higher number of adhesive leukocytes in noise-exposed wild type mice. Dorsal microvascular diameter (by trend), red blood cell velocity, and segmental blood flow were also decreased by noise exposure indicating microvascular constriction. All adverse effects on functional parameters were normalized or improved at least by trend in noise-exposed gp91phox−/y mice. Noise exposure also induced endothelial dysfunction in cerebral microvessels, which was associated with higher oxidative stress burden and inflammation, as measured using video microscopy. We here establish a link between a pro-inflammatory phenotype of plasma, activation of circulating leukocytes and microvascular dysfunction in mice exposed to aircraft noise. The phagocytic NADPH oxidase was identified as a central player in the underlying pathophysiological mechanisms.

ACS Style

Jonas Eckrich; Katie Frenis; Giovanny Rodriguez-Blanco; Yue Ruan; Subao Jiang; Maria Teresa Bayo Jimenez; Marin Kuntic; Matthias Oelze; Omar Hahad; Huige Li; Adrian Gericke; Sebastian Steven; Sebastian Strieth; Alex von Kriegsheim; Thomas Münzel; Benjamin Philipp Ernst; Andreas Daiber. Aircraft noise exposure drives the activation of white blood cells and induces microvascular dysfunction in mice. Redox Biology 2021, 46, 102063 .

AMA Style

Jonas Eckrich, Katie Frenis, Giovanny Rodriguez-Blanco, Yue Ruan, Subao Jiang, Maria Teresa Bayo Jimenez, Marin Kuntic, Matthias Oelze, Omar Hahad, Huige Li, Adrian Gericke, Sebastian Steven, Sebastian Strieth, Alex von Kriegsheim, Thomas Münzel, Benjamin Philipp Ernst, Andreas Daiber. Aircraft noise exposure drives the activation of white blood cells and induces microvascular dysfunction in mice. Redox Biology. 2021; 46 ():102063.

Chicago/Turabian Style

Jonas Eckrich; Katie Frenis; Giovanny Rodriguez-Blanco; Yue Ruan; Subao Jiang; Maria Teresa Bayo Jimenez; Marin Kuntic; Matthias Oelze; Omar Hahad; Huige Li; Adrian Gericke; Sebastian Steven; Sebastian Strieth; Alex von Kriegsheim; Thomas Münzel; Benjamin Philipp Ernst; Andreas Daiber. 2021. "Aircraft noise exposure drives the activation of white blood cells and induces microvascular dysfunction in mice." Redox Biology 46, no. : 102063.

Review
Published: 06 July 2021 in International Journal of Molecular Sciences
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Despite extensive efforts to combat cigarette smoking/tobacco use, it still remains a leading cause of global morbidity and mortality, killing more than eight million people each year. While tobacco smoking is a major risk factor for non-communicable diseases related to the four main groups—cardiovascular disease, cancer, chronic lung disease, and diabetes—its impact on neuropsychiatric risk is rather elusive. The aim of this review article is to emphasize the importance of smoking as a potential risk factor for neuropsychiatric disease and to identify central pathophysiological mechanisms that may contribute to this relationship. There is strong evidence from epidemiological and experimental studies indicating that smoking may increase the risk of various neuropsychiatric diseases, such as dementia/cognitive decline, schizophrenia/psychosis, depression, anxiety disorder, and suicidal behavior induced by structural and functional alterations of the central nervous system, mainly centered on inflammatory and oxidative stress pathways. From a public health perspective, preventive measures and policies designed to counteract the global epidemic of smoking should necessarily include warnings and actions that address the risk of neuropsychiatric disease.

ACS Style

Omar Hahad; Andreas Daiber; Matthias Michal; Marin Kuntic; Klaus Lieb; Manfred Beutel; Thomas Münzel. Smoking and Neuropsychiatric Disease—Associations and Underlying Mechanisms. International Journal of Molecular Sciences 2021, 22, 7272 .

AMA Style

Omar Hahad, Andreas Daiber, Matthias Michal, Marin Kuntic, Klaus Lieb, Manfred Beutel, Thomas Münzel. Smoking and Neuropsychiatric Disease—Associations and Underlying Mechanisms. International Journal of Molecular Sciences. 2021; 22 (14):7272.

Chicago/Turabian Style

Omar Hahad; Andreas Daiber; Matthias Michal; Marin Kuntic; Klaus Lieb; Manfred Beutel; Thomas Münzel. 2021. "Smoking and Neuropsychiatric Disease—Associations and Underlying Mechanisms." International Journal of Molecular Sciences 22, no. 14: 7272.

Journal article
Published: 04 June 2021 in Nitric Oxide
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Arterial hypertension is one of the major health risk factors leading to coronary artery disease, stroke or peripheral artery disease. Dietary uptake of inorganic nitrite (NO2−) and nitrate (NO3−) via vegetables leads to enhanced vascular NO bioavailability and provides antihypertensive effects. The present study aims to understand the underlying vasoprotective effects of nutritional NO2− and NO3− co-therapy in mice with angiotensin-II (AT-II)-induced arterial hypertension. High-dose AT-II (1 mg/kg/d, 1w, s. c.) was used to induce arterial hypertension in male C57BL/6 mice. Additional inorganic nitrite (7.5 mg/kg/d, p. o.) or nitrate (150 mg/kg/d, p. o.) were administered via the drinking water. Blood pressure (tail-cuff method) and endothelial function (isometric tension) were determined. Oxidative stress and inflammation markers were quantified in aorta, heart, kidney and blood. Co-treatment with inorganic nitrite, but not with nitrate, normalized vascular function, oxidative stress markers and inflammatory pathways in AT-II treated mice. Of note, the highly beneficial effects of nitrite on all parameters and the less pronounced protection by nitrate, as seen by improvement of some parameters, were observed despite no significant increase in plasma nitrite levels by both therapies. Methemoglobin levels tended to be higher upon nitrite/nitrate treatment. Nutritional nitric oxide precursors represent a non-pharmacological treatment option for hypertension that could be applied to the general population (e.g. by eating certain vegetables). The more beneficial effects of inorganic nitrite may rely on superior NO bioactivation and stronger blood pressure lowering effects. Future large-scale clinical studies should investigate whether hypertension and cardiovascular outcome in general can be influenced by dietary inorganic nitrite therapy.

ACS Style

Paul Stamm; Matthias Oelze; Sebastian Steven; Swenja Kröller-Schön; Miroslava Kvandova; Sanela Kalinovic; Agnieszka Jasztal; Agnieszka Kij; Marin Kuntic; Maria Teresa Bayo Jimenez; Bartosz Proniewski; Huige Li; Eberhard Schulz; Stefan Chlopicki; Andreas Daiber; Thomas Münzel. Direct comparison of inorganic nitrite and nitrate on vascular dysfunction and oxidative damage in experimental arterial hypertension. Nitric Oxide 2021, 113-114, 57 -69.

AMA Style

Paul Stamm, Matthias Oelze, Sebastian Steven, Swenja Kröller-Schön, Miroslava Kvandova, Sanela Kalinovic, Agnieszka Jasztal, Agnieszka Kij, Marin Kuntic, Maria Teresa Bayo Jimenez, Bartosz Proniewski, Huige Li, Eberhard Schulz, Stefan Chlopicki, Andreas Daiber, Thomas Münzel. Direct comparison of inorganic nitrite and nitrate on vascular dysfunction and oxidative damage in experimental arterial hypertension. Nitric Oxide. 2021; 113-114 ():57-69.

Chicago/Turabian Style

Paul Stamm; Matthias Oelze; Sebastian Steven; Swenja Kröller-Schön; Miroslava Kvandova; Sanela Kalinovic; Agnieszka Jasztal; Agnieszka Kij; Marin Kuntic; Maria Teresa Bayo Jimenez; Bartosz Proniewski; Huige Li; Eberhard Schulz; Stefan Chlopicki; Andreas Daiber; Thomas Münzel. 2021. "Direct comparison of inorganic nitrite and nitrate on vascular dysfunction and oxidative damage in experimental arterial hypertension." Nitric Oxide 113-114, no. : 57-69.

Journal article
Published: 19 April 2021 in Antioxidants
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Vascular oxidative stress, inflammation, and subsequent endothelial dysfunction are consequences of traditional cardiovascular risk factors, all of which contribute to cardiovascular disease. Environmental stressors, such as traffic noise and air pollution, may also facilitate the development and progression of cardiovascular and metabolic diseases. In our previous studies, we investigated the influence of aircraft noise exposure on molecular mechanisms, identifying oxidative stress and inflammation as central players in mediating vascular function. The present study investigates the role of heme oxygenase-1 (HO-1) as an antioxidant response preventing vascular consequences following exposure to aircraft noise. C57BL/6J mice were treated with the HO-1 inducer hemin (25 mg/kg i.p.) or the NRF2 activator dimethyl fumarate (DMF, 20 mg/kg p.o.). During therapy, the animals were exposed to noise at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A). Our data showed a marked protective effect of both treatments on animals exposed to noise for 4 days by normalization of arterial hypertension and vascular dysfunction in the noise-exposed groups. We observed a partial normalization of noise-triggered oxidative stress and inflammation by hemin and DMF therapy, which was associated with HO-1 induction. The present study identifies possible new targets for the mitigation of the adverse health effects caused by environmental noise exposure. Since natural dietary constituents can achieve HO-1 and NRF2 induction, these pathways represent promising targets for preventive measures.

ACS Style

Maria Bayo Jimenez; Katie Frenis; Swenja Kröller-Schön; Marin Kuntic; Paul Stamm; Miroslava Kvandová; Matthias Oelze; Huige Li; Sebastian Steven; Thomas Münzel; Andreas Daiber. Noise-Induced Vascular Dysfunction, Oxidative Stress, and Inflammation Are Improved by Pharmacological Modulation of the NRF2/HO-1 Axis. Antioxidants 2021, 10, 625 .

AMA Style

Maria Bayo Jimenez, Katie Frenis, Swenja Kröller-Schön, Marin Kuntic, Paul Stamm, Miroslava Kvandová, Matthias Oelze, Huige Li, Sebastian Steven, Thomas Münzel, Andreas Daiber. Noise-Induced Vascular Dysfunction, Oxidative Stress, and Inflammation Are Improved by Pharmacological Modulation of the NRF2/HO-1 Axis. Antioxidants. 2021; 10 (4):625.

Chicago/Turabian Style

Maria Bayo Jimenez; Katie Frenis; Swenja Kröller-Schön; Marin Kuntic; Paul Stamm; Miroslava Kvandová; Matthias Oelze; Huige Li; Sebastian Steven; Thomas Münzel; Andreas Daiber. 2021. "Noise-Induced Vascular Dysfunction, Oxidative Stress, and Inflammation Are Improved by Pharmacological Modulation of the NRF2/HO-1 Axis." Antioxidants 10, no. 4: 625.

Review
Published: 28 February 2021 in International Journal of Molecular Sciences
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The World Health Organization estimates that only approximately 25% of diversity in longevity is explained by genetic factors, while the other 75% is largely determined by interactions with the physical and social environments. Indeed, aging is a multifactorial process that is influenced by a range of environmental, sociodemographic, and biopsychosocial factors, all of which might act in concert to determine the process of aging. The global average life expectancy increased fundamentally over the past century, toward an aging population, correlating with the development and onset of age-related diseases, mainly from cardiovascular and neurological nature. Therefore, the identification of determinants of healthy and unhealthy aging is a major goal to lower the burden and socioeconomic costs of age-related diseases. The role of environmental factors (such as air pollution and noise exposure) as crucial determinants of the aging process are being increasingly recognized. Here, we critically review recent findings concerning the pathomechanisms underlying the aging process and their correlates in cardiovascular and neurological disease, centered on oxidative stress and inflammation, as well as the influence of prominent environmental pollutants, namely air pollution and traffic noise exposure, which is suggested to accelerate the aging process. Insight into these types of relationships and appropriate preventive strategies are urgently needed to promote healthy aging.

ACS Style

Omar Hahad; Katie Frenis; Marin Kuntic; Andreas Daiber; Thomas Münzel. Accelerated Aging and Age-Related Diseases (CVD and Neurological) Due to Air Pollution and Traffic Noise Exposure. International Journal of Molecular Sciences 2021, 22, 2419 .

AMA Style

Omar Hahad, Katie Frenis, Marin Kuntic, Andreas Daiber, Thomas Münzel. Accelerated Aging and Age-Related Diseases (CVD and Neurological) Due to Air Pollution and Traffic Noise Exposure. International Journal of Molecular Sciences. 2021; 22 (5):2419.

Chicago/Turabian Style

Omar Hahad; Katie Frenis; Marin Kuntic; Andreas Daiber; Thomas Münzel. 2021. "Accelerated Aging and Age-Related Diseases (CVD and Neurological) Due to Air Pollution and Traffic Noise Exposure." International Journal of Molecular Sciences 22, no. 5: 2419.

Journal article
Published: 26 October 2020 in Antioxidants
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Background: The superoxide-generating enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2 or gp91phox, the phagocytic isoform) was reported as a major source of oxidative stress in various human diseases. Genetic deletion is widely used to study the impact of NOX2-derived reactive oxygen species (ROS) on disease development and progression in various animal models. Here, we investigate why NOX2 knockout mice show no NOX2 activity but express NOX2 mRNA and protein. Methods and Results: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Protein expression was still detectable in different tissues of the NOX2 knockout mice, at the expected and a slightly lower molecular weight (determined by Western blot). The NOX2 gene was even largely enhanced at its expressional level in NOX2 knockout mice. RNA sequencing revealed a modified NOX2 mRNA in the knockout mice that is obviously translated to a truncated inactive mutant enzyme. Conclusion: Although the commercial NOX2 knockout mice display no considerable enzymatic NOX2 activity, expression of the NOX2 gene (when using standard primers) and protein (when using antibodies binding to the carboxy-terminal end) can still be detected, which may lead to confusion among investigators.

ACS Style

Monika Göllner; Irmgard Ihrig-Biedert; Victoria Petermann; Sabrina Saurin; Matthias Oelze; Swenja Kröller-Schön; Ksenija Vujacic-Mirski; Marin Kuntic; Andrea Pautz; Andreas Daiber; Hartmut Kleinert. NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein. Antioxidants 2020, 9, 1043 .

AMA Style

Monika Göllner, Irmgard Ihrig-Biedert, Victoria Petermann, Sabrina Saurin, Matthias Oelze, Swenja Kröller-Schön, Ksenija Vujacic-Mirski, Marin Kuntic, Andrea Pautz, Andreas Daiber, Hartmut Kleinert. NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein. Antioxidants. 2020; 9 (11):1043.

Chicago/Turabian Style

Monika Göllner; Irmgard Ihrig-Biedert; Victoria Petermann; Sabrina Saurin; Matthias Oelze; Swenja Kröller-Schön; Ksenija Vujacic-Mirski; Marin Kuntic; Andrea Pautz; Andreas Daiber; Hartmut Kleinert. 2020. "NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein." Antioxidants 9, no. 11: 1043.

Review
Published: 23 August 2020 in Expert Review of Respiratory Medicine
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E-cigarettes have become a controversial topic. While their benefits are questioned by the scientific community, a part of the medical profession is still supporting them as an effective harm reduction tool for smoking cessation. The impact of E-cigarettes on the cardiovascular system is still elusive. We assessed results from animal, pre(clinical), and epidemiological studies to critically evaluate and synthesize evidence relevant to the cardiovascular effects of E-cigarettes. Animal studies have demonstrated that E-cigarette vapor exposure can cause endothelial and cardiac dysfunction. However, there have also been reports on the less harmful effects of E-cigarette vapor exposure in comparison to classical tobacco cigarettes. Measurements of flow-mediated dilation in acute human exposure settings have mostly demonstrated that E-cigarettes cause vascular endothelial dysfunction. Long term epidemiological studies have shown that E-cigarette use is associated with an increased risk for cardiovascular disease, although switching from classical tobacco cigarettes to E-cigarettes can have beneficial cardiovascular effects. Misinterpretation of scientific data by activists on either side is another problem. In conclusion, we need more and better (pre)clinical data comparing the health effects of E-cigarette vaping as compared with tobacco cigarette smoking, in order to counsel the legislation for better health policies.

ACS Style

Marin Kuntic; Omar Hahad; Andreas Daiber; Thomas Münzel. Could E-cigarette vaping contribute to heart disease? Expert Review of Respiratory Medicine 2020, 14, 1131 -1139.

AMA Style

Marin Kuntic, Omar Hahad, Andreas Daiber, Thomas Münzel. Could E-cigarette vaping contribute to heart disease? Expert Review of Respiratory Medicine. 2020; 14 (11):1131-1139.

Chicago/Turabian Style

Marin Kuntic; Omar Hahad; Andreas Daiber; Thomas Münzel. 2020. "Could E-cigarette vaping contribute to heart disease?" Expert Review of Respiratory Medicine 14, no. 11: 1131-1139.

Journal article
Published: 21 July 2020 in European Heart Journal
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Thomas Münzel and co-authors report from Mainz on the pros and cons of e-cigarette smoking

ACS Style

Thomas Münzel; Marin Kuntic; Sebastian Steven; Omar Hahad; Andreas Daiber. Is vaping better than smoking cigarettes? European Heart Journal 2020, 41, 2612 -2614.

AMA Style

Thomas Münzel, Marin Kuntic, Sebastian Steven, Omar Hahad, Andreas Daiber. Is vaping better than smoking cigarettes? European Heart Journal. 2020; 41 (28):2612-2614.

Chicago/Turabian Style

Thomas Münzel; Marin Kuntic; Sebastian Steven; Omar Hahad; Andreas Daiber. 2020. "Is vaping better than smoking cigarettes?" European Heart Journal 41, no. 28: 2612-2614.

Journal article
Published: 25 June 2020 in European Heart Journal
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Tobacco smoking is a leading cause of non-communicable disease globally and is a major risk factor for cardiovascular disease (CVD) and lung disease. Importantly, recent data by the World Health Organizations (WHO) indicate that in the last two decades global tobacco use has significantly dropped, which was largely driven by decreased numbers of female smokers. Despite such advances, the use of e-cigarettes and waterpipes (shisha, hookah, narghile) is an emerging trend, especially among younger generations. There is growing body of evidence that e-cigarettes are not a harm-free alternative to tobacco cigarettes and there is considerable debate as to whether e-cigarettes are saving smokers or generating new addicts. Here, we provide an updated overview of the impact of tobacco/waterpipe (shisha) smoking and e-cigarette vaping on endothelial function, a biomarker for early, subclinical, atherosclerosis from human and animal studies. Also their emerging adverse effects on the proteome, transcriptome, epigenome, microbiome, and the circadian clock are summarized. We briefly discuss heat-not-burn tobacco products and their cardiovascular health effects. We discuss the impact of the toxic constituents of these products on endothelial function and subsequent CVD and we also provide an update on current recommendations, regulation and advertising with focus on the USA and Europe. As outlined by the WHO, tobacco cigarette, waterpipe, and e-cigarette smoking/vaping may contribute to an increased burden of symptoms due to coronavirus disease 2019 (COVID-19) and to severe health consequences.

ACS Style

Thomas Münzel; Omar Hahad; Marin Kuntic; John F Keaney; John E Deanfield; Andreas Daiber. Effects of tobacco cigarettes, e-cigarettes, and waterpipe smoking on endothelial function and clinical outcomes. European Heart Journal 2020, 41, 4057 -4070.

AMA Style

Thomas Münzel, Omar Hahad, Marin Kuntic, John F Keaney, John E Deanfield, Andreas Daiber. Effects of tobacco cigarettes, e-cigarettes, and waterpipe smoking on endothelial function and clinical outcomes. European Heart Journal. 2020; 41 (41):4057-4070.

Chicago/Turabian Style

Thomas Münzel; Omar Hahad; Marin Kuntic; John F Keaney; John E Deanfield; Andreas Daiber. 2020. "Effects of tobacco cigarettes, e-cigarettes, and waterpipe smoking on endothelial function and clinical outcomes." European Heart Journal 41, no. 41: 4057-4070.

Journal article
Published: 25 March 2020 in European Heart Journal
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ACS Style

Marin Kuntic; Andreas Daiber; Thomas Münzel. Acrolein, e-cigarettes, and pulmonary and vascular damage. European Heart Journal 2020, 41, 1524 -1524.

AMA Style

Marin Kuntic, Andreas Daiber, Thomas Münzel. Acrolein, e-cigarettes, and pulmonary and vascular damage. European Heart Journal. 2020; 41 (15):1524-1524.

Chicago/Turabian Style

Marin Kuntic; Andreas Daiber; Thomas Münzel. 2020. "Acrolein, e-cigarettes, and pulmonary and vascular damage." European Heart Journal 41, no. 15: 1524-1524.

Journal article
Published: 13 November 2019 in European Heart Journal
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Aims Electronic (e)-cigarettes have been marketed as a ‘healthy’ alternative to traditional combustible cigarettes and as an effective method of smoking cessation. There are, however, a paucity of data to support these claims. In fact, e-cigarettes are implicated in endothelial dysfunction and oxidative stress in the vasculature and the lungs. The mechanisms underlying these side effects remain unclear. Here, we investigated the effects of e-cigarette vapour on vascular function in smokers and experimental animals to determine the underlying mechanisms. Methods and results Acute e-cigarette smoking produced a marked impairment of endothelial function in chronic smokers determined by flow-mediated dilation. In mice, e-cigarette vapour without nicotine had more detrimental effects on endothelial function, markers of oxidative stress, inflammation, and lipid peroxidation than vapour containing nicotine. These effects of e-cigarette vapour were largely absent in mice lacking phagocytic NADPH oxidase (NOX-2) or upon treatment with the endothelin receptor blocker macitentan or the FOXO3 activator bepridil. We also established that the e-cigarette product acrolein, a reactive aldehyde, recapitulated many of the NOX-2-dependent effects of e-cigarette vapour using in vitro blood vessel incubation. Conclusions E-cigarette vapour exposure increases vascular, cerebral, and pulmonary oxidative stress via a NOX-2-dependent mechanism. Our study identifies the toxic aldehyde acrolein as a key mediator of the observed adverse vascular consequences. Thus, e-cigarettes have the potential to induce marked adverse cardiovascular, pulmonary, and cerebrovascular consequences. Since e-cigarette use is increasing, particularly amongst youth, our data suggest that aggressive steps are warranted to limit their health risks.

ACS Style

Marin Kuntic; Matthias Oelze; Sebastian Steven; Swenja Kröller-Schön; Paul Stamm; Sanela Kalinovic; Katie Frenis; Ksenija Vujacic-Mirski; Maria Teresa Bayo Jimenez; Miroslava Kvandova; Konstantina Filippou; Ahmad Al Zuabi; Vivienne Brückl; Omar Hahad; Steffen Daub; Franco Varveri; Tommaso Gori; Regina Huesmann; Thorsten Hoffmann; Frank P Schmidt; John F Keaney; Andreas Daiber; Thomas Münzel. Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2). European Heart Journal 2019, 41, 2472 -2483.

AMA Style

Marin Kuntic, Matthias Oelze, Sebastian Steven, Swenja Kröller-Schön, Paul Stamm, Sanela Kalinovic, Katie Frenis, Ksenija Vujacic-Mirski, Maria Teresa Bayo Jimenez, Miroslava Kvandova, Konstantina Filippou, Ahmad Al Zuabi, Vivienne Brückl, Omar Hahad, Steffen Daub, Franco Varveri, Tommaso Gori, Regina Huesmann, Thorsten Hoffmann, Frank P Schmidt, John F Keaney, Andreas Daiber, Thomas Münzel. Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2). European Heart Journal. 2019; 41 (26):2472-2483.

Chicago/Turabian Style

Marin Kuntic; Matthias Oelze; Sebastian Steven; Swenja Kröller-Schön; Paul Stamm; Sanela Kalinovic; Katie Frenis; Ksenija Vujacic-Mirski; Maria Teresa Bayo Jimenez; Miroslava Kvandova; Konstantina Filippou; Ahmad Al Zuabi; Vivienne Brückl; Omar Hahad; Steffen Daub; Franco Varveri; Tommaso Gori; Regina Huesmann; Thorsten Hoffmann; Frank P Schmidt; John F Keaney; Andreas Daiber; Thomas Münzel. 2019. "Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2)." European Heart Journal 41, no. 26: 2472-2483.

Review article
Published: 23 June 2019 in Oxidative Medicine and Cellular Longevity
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Cardiovascular disease is a leading cause of death and reduced quality of life, proven by the latest data of the Global Burden of Disease Study, and is only gaining in prevalence worldwide. Clinical trials have identified chronic inflammatory disorders as cardiovascular risks, and recent research has revealed a contribution by various inflammatory cells to vascular oxidative stress. Atherosclerosis and cardiovascular disease are closely associated with inflammation, probably due to the close interaction of inflammation with oxidative stress. Classical therapies for inflammatory disorders have demonstrated protective effects in various models of cardiovascular disease; especially established drugs with pleiotropic immunomodulatory properties have proven beneficial cardiovascular effects; normalization of oxidative stress seems to be a common feature of these therapies. The close link between inflammation and redox balance was also supported by reports on aggravated inflammatory phenotype in the absence of antioxidant defense proteins (e.g., superoxide dismutases, heme oxygenase-1, and glutathione peroxidases) or overexpression of reactive oxygen species producing enzymes (e.g., NADPH oxidases). The value of immunomodulation for the treatment of cardiovascular disease was recently supported by large-scale clinical trials demonstrating reduced cardiovascular mortality in patients with established atherosclerotic disease when treated by highly specific anti-inflammatory therapies (e.g., using monoclonal antibodies against cytokines). Modern antidiabetic cardiovascular drugs (e.g., SGLT2 inhibitors, DPP-4 inhibitors, and GLP-1 analogs) seem to share these immunomodulatory properties and display potent antioxidant effects, all of which may explain their successful lowering of cardiovascular risk.

ACS Style

Sebastian Steven; Katie Frenis; Matthias Oelze; Sanela Kalinovic; Marin Kuntic; Maria Teresa Bayo Jimenez; Ksenija Vujacic-Mirski; Johanna Helmstädter; Swenja Kröller-Schön; Thomas Münzel; Andreas Daiber. Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease. Oxidative Medicine and Cellular Longevity 2019, 2019, 1 -26.

AMA Style

Sebastian Steven, Katie Frenis, Matthias Oelze, Sanela Kalinovic, Marin Kuntic, Maria Teresa Bayo Jimenez, Ksenija Vujacic-Mirski, Johanna Helmstädter, Swenja Kröller-Schön, Thomas Münzel, Andreas Daiber. Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease. Oxidative Medicine and Cellular Longevity. 2019; 2019 ():1-26.

Chicago/Turabian Style

Sebastian Steven; Katie Frenis; Matthias Oelze; Sanela Kalinovic; Marin Kuntic; Maria Teresa Bayo Jimenez; Ksenija Vujacic-Mirski; Johanna Helmstädter; Swenja Kröller-Schön; Thomas Münzel; Andreas Daiber. 2019. "Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease." Oxidative Medicine and Cellular Longevity 2019, no. : 1-26.

Review article
Published: 02 April 2019 in BioFactors
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Environmental noise is a well‐recognized health risk and part of the external exposome—the World Health Organization estimates that 1 million healthy life years are lost annually in Western Europe alone due to noise‐related complications, including increased incidence of hypertension, heart failure, myocardial infarction, and stroke. Previous data suggest that noise works through two paired pathways in a proposed reaction model for noise exposure. As a nonspecific stressor, chronic low‐level noise exposure can cause a disruption of sleep and communication leading to annoyance and subsequent sympathetic and endocrine stress responses leading to increased blood pressure, heart rate, stress hormone levels, and in particular more oxidative stress, being responsible for vascular dysfunction and representing changes of the internal exposome. Chronic stress generates cardiovascular risk factors on its own such as increased blood pressure, blood viscosity, blood glucose, and activation of blood coagulation. To this end, persistent chronic noise exposure increases cardiometabolic diseases, including arterial hypertension, coronary artery disease, arrhythmia, heart failure, diabetes mellitus type 2, and stroke. The present review discusses the mechanisms of the nonauditory noise‐induced cardiovascular and metabolic consequences, focusing on mental stress signaling pathways, activation of the hypothalamic–pituitary–adrenocortical axis and sympathetic nervous system, the association of these activations with inflammation, and the subsequent onset of oxidative stress and vascular dysfunction. © 2019 BioFactors, 2019

ACS Style

Andreas Daiber; Swenja Kröller‐Schön; Katie Frenis; Matthias Oelze; Sanela Kalinovic; Ksenija Vujacic‐Mirski; Marin Kuntic; Maria Teresa Bayo Jimenez; Johanna Helmstädter; Sebastian Steven; Bato Korac; Thomas Münzel. Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction—Signatures of the internal exposome. BioFactors 2019, 45, 495 -506.

AMA Style

Andreas Daiber, Swenja Kröller‐Schön, Katie Frenis, Matthias Oelze, Sanela Kalinovic, Ksenija Vujacic‐Mirski, Marin Kuntic, Maria Teresa Bayo Jimenez, Johanna Helmstädter, Sebastian Steven, Bato Korac, Thomas Münzel. Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction—Signatures of the internal exposome. BioFactors. 2019; 45 (4):495-506.

Chicago/Turabian Style

Andreas Daiber; Swenja Kröller‐Schön; Katie Frenis; Matthias Oelze; Sanela Kalinovic; Ksenija Vujacic‐Mirski; Marin Kuntic; Maria Teresa Bayo Jimenez; Johanna Helmstädter; Sebastian Steven; Bato Korac; Thomas Münzel. 2019. "Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction—Signatures of the internal exposome." BioFactors 45, no. 4: 495-506.