Role of oxidative stress in cardiovascular diseases

By N. Dhalla, R. Temsah, T. Netticadan. Journal of Hypertension, 2000

1,518 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/413d948d7be294c3019a92ecc1a0b0d3ebafbfbe

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In Cardiology and Cardiovascular Medicine

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In Molecular Biology

In Pathology and Forensic Medicine

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Citations in the corpus

A review on the dietary flavonoid kaempferol. (2011, background): “Because oxidative stress [231] and inflammation [232] are known cardiovascular risk factors, it makes sense to think that the known antioxidant and anti-inflammatory properties of kaempferol may play a critical role in this protective effect.”
Exposure Assessment for Atmospheric Ultrafine Particles (UFPs) and Implications in Epidemiologic Research (2005, background): “Evidence for the importance of oxidant stress responses to cardiovascular effects is that antioxidant therapy is protective against the development of hypertension, aetherosclerosis, cardiomyopathies, coronary heart disease, and congestive heart failure (Dhalla et al. 2000).”
Reactive oxygen species in vascular biology: implications in hypertension (2004, neutral): “…Ca2+ channel blockers, ACE inhibitors, and AT1 receptor blockers, downregulate expression of oxidase subunits and decrease NAD(P)H oxidase activity (Dandona et al. 2000; Dhalla et al. 2000; Mantle et al. 2000; Ohtahara et al. 2001; Taddei et al. 2001; Diep et al. 2002; Wassman et al. 2002).”
The Effect of Fine and Coarse Particulate Air Pollution on Mortality: A National Analysis (2009, background): “Animal experiments indicate that reactive oxygen species, which have established relevance in the pathogenesis of CVD and aging (Dhalla et al. 2000), are affected by particles, which represents one pathway for their cardiovascular and lung effects (Brook et al. 2004; Gurgueira et al. 2002; Nel…”
Mitochondrial dysfunction and oxidative stress in metabolic disorders - A Step towards mitochondria based therapeutic strategies (2016, background): “The excess of ROS leads to cellular injury and declined antioxidant capacity, which seems to be due to defects in mitochondrial functions and mtDNA damage, endothelial dysfunction and altered gene expression [6].”
Doxorubicin-induced cardiomyopathy: from molecular mechanisms to therapeutic strategies. (2012, neutral): “Perhaps, most critically for the myocardium, ROS can induce the release of Ca 2+ ions [50].”
Understanding ultrasound induced sonoporation: definitions and underlying mechanisms. (2014, background): “The second possibility is that reactive oxygen species (ROS) induce cellular injury via lipid peroxidation which can result in lipid bilayer rearrangement and membrane disruption [54] (Fig.”
Free radicals and antioxidants in normal physiological functions and human disease. (2007, background): “The ROS-induced oxidative stress in cardiac and vascular myocytes has been linked with cardiovascular tissue injury (Dhalla et al., 2000).”
Increased myocardial NADPH oxidase activity in human heart failure. (2003, background): “Increased oxidative stress may contribute to contractile dysfunction, endothelial dysfunction, myocyte apoptosis and necrosis, remodeling of the extracellular matrix, and the progressive downward spiral of heart failure (1,2).”
Therapeutic Potential of Moringa oleifera Leaves in Chronic Hyperglycemia and Dyslipidemia: A Review (2012, background): “Oxidative stress is widely accepted as a major contributing factor in the pathogenesis of CVD and diabetes (Dhalla et al., 2000; Kaneto et al., 2007; Rodrigo et al., 2011).”