Background: Major depression (MD) has been associated with increased cardiovascular mortality in patients with coronary heart disease (CHD) and has been described as an independent risk factor for the development of CHD in healthy subjects; however, the mechanism of the association between MD and CHD remains to be determined. Nitric oxide (NO) plays a major role in cardiovascular regulation, and decreased NO production has been associated with several cardiovascular risk factors. We hypothesized that in patients with MD, NO production by both platelets and the endothelium would be reduced when compared with healthy control subjects (HCs).
Methods: Blood samples were obtained from 15 subjects with MD and 16 HCs with no known history of cardiovascular illness. Plasma NO metabolite (NOx) levels were analyzed by chemiluminescence. Platelet endothelial NO synthase (eNOS) activity was examined through the conversion of l-[(14)C]arginine to l-[(14)C]citrulline.
Results: The levels of both plasma NOx and platelet eNOS activity were significantly lower in subjects with MD compared with HCs.
Conclusions: These data suggest that decreased NO production by the vascular wall and platelets might contribute to the increased CHD risk observed in patients with MD.
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http://dx.doi.org/10.1016/j.biopsych.2004.03.003 | DOI Listing |
Front Pharmacol
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Department of Cardiovascular Center, First Affiliated Hospital of Huzhou University, Huzhou, China.
The emergence of targeted anti-tumor drugs has significantly prolonged the lifespan and improved the prognosis of cancer patients. Among these drugs, vascular endothelial growth factor (VEGF) inhibitors, particularly novel small molecule tyrosine kinase inhibitors (TKIs), are extensively employed as VEGF inhibitors; however, they are also associated with a higher incidence of complications, with hypertension being the most prevalent cardiovascular toxic side effect. Currently, it is widely accepted that TKIs-induced hypertension involves multiple mechanisms including dysregulation of the endothelin (ET) axis, reduced bioavailability of nitric oxide (NO), imbalance in NO-ROS equilibrium system, vascular rarefaction, and activation of epithelial sodium calcium channels; nevertheless, excessive activation of ET system appears to be predominantly responsible for this condition.
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Department of Geriatric Medicine, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China.
Endothelial cell dysfunction plays a crucial role in the early development of cerebral small vessel disease (CSVD). Arginase-1 (ARG1) is expressed in endothelial cells, and its deficiency may exacerbate cerebrovascular damage by increasing reactive oxygen species (ROS) production, thereby inducing endothelial cell apoptosis. Berbamine (BBM) has shown potential in neuroprotection and cardiovascular disease prevention.
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January 2025
School of Kinesiology, Auburn University, Auburn, AL, United States.
Nitric oxide (NO) is a ubiquitous signaling molecule known to modulate various physiological processes, with specific implications in skeletal muscle and broader applications in exercise performance. This review focuses on the modulation of skeletal muscle function, mitochondrial adaptation and function, redox state by NO, and the effect of nitrate supplementation on exercise performance. In skeletal muscle function, NO is believed to increase the maximal shortening velocity and peak power output of muscle fibers.
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Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, Busan 49315, Republic of Korea.
Inflammatory is a crucial part of the immune system of body protect it from harmful invaders, such as bacteria, viruses, and other foreign substances. In this study, the effects of chloroform extract of fermented (CEFV) on lipopolysaccharide (LPS)-induced inflammatory response in RAW264.7 macrophages were investigated.
View Article and Find Full Text PDFJ Nanobiotechnology
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School of Life Sciences, Faculty of Medicine, Tianjin University, Tianjin, 300072, China.
Oxidative stress and inflammatory dysregulation play crucial roles in pathogenesis of acute lung injury (ALI), and their cyclic synergy drives excessive inflammatory responses and further exacerbates ALI. Therefore, new effective strategies to treat ALI are urgently needed. Herein, a novel synergistic selenium based chlorogenic acid nanoparticle was developed to disrupt the cyclic synergistic effect between oxidative stress and inflammatory response in ALI.
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