Reactive oxygen species (ROS) such as superoxide and H<sub>2</sub>O<sub>2</sub> derived from NADPH oxidases have been implicated in the pathogenesis of cardiovascular diseases.
NADPH oxidase-derived superoxide (O<sub>2</sub><sup>-</sup>) generation is usually considered as an important factor to the pathogenesis of cardiovascular diseases.
Previous studies have demonstrated that NADPH oxidase (NOX)/vascular peroxidase (VPO1) pathway - mediated oxidative stress plays an important role in the pathogenesis of multiple cardiovascular diseases.
Accumulating evidence demonstrates that vascular oxidative stress is a critical feature of atherosclerotic process, potentially triggered by several infectious agents that are considered as risk co-factors for the atherosclerotic cardiovascular diseases (CVDs).<i>C. pneumoniae</i> has been shown to upregulate multiple enzymatic systems capable of producing reactive oxygen species (ROS) such as NADPH oxidase (NOX) and cyclooxygenase in vascular endothelial cells, NOX and cytochrome c oxidase in macrophages as well as nitric oxide synthase and lipoxygenase in platelets contributing to both early and late stages of atherosclerosis.<i>P. gingivalis</i> seems to be markedly involved in the atherosclerotic process as compared to <i>A. actinomycetemcomitans</i> contributing to LDL oxidation and foam cell formation.
Increased activity of NADPH oxidases has been implicated in various pathologies, including cardiovascular disease, neurological dysfunction, and cancer.
A significant source of reactive oxygen species production and oxidative stress in cardiovascular disease is the family of NADPH oxidases that contribute to several pathologies.
The action of indoxyl sulfate are related to multiple NADPH oxidase-mediated redox signaling pathways, which have been implicated in the pathophysiology of different forms of CVD, including chronic heart failure, arrhythmia, atherosclerotic vascular disease and coronary calcification.
Moreover, the observed protective effects of apocynin in BAECs suggest the potential involvement of NADPH-oxidase in MeHg-induced endothelial dysfunction, which represents a pivotal event in most cardiovascular diseases.
This screening system and delivery method could have broader implications for miRNA-mediated therapeutics for cardiovascular and other diseases.<b>NEW & NOTEWORTHY</b> NADPH oxidase (Nox)2 is a promising target for treating cardiovascular disease, but there are no specific inhibitors.
Excessive levels of reactive oxygen species (ROS) and increased expression of NADPH oxidases (Nox) have been proposed to contribute to pulmonary artery hypertension (PAH) and other cardiovascular diseases (CVD).
Additional high-resolution studies in multiple vascular beds are required to address the therapeutic potential of NADPH oxidase inhibition in cardiovascular diseases.
ROS generated by NADPH oxidase, mitochondrial electron transport chain, and proinflammatory cytokines activates mitogen-activated protein kinases and transcription factors, which in turn modulate ion channel functions and ultimately increase neuronal activity and sympathetic outflow in brain Ang II-dependent cardiovascular diseases.
These results suggest that assessment of the C242T CYBA polymorphism of the NADPH oxidase may be useful in identifying the risk for developing cardiovascular disease in ESRD patients.
Common genetic polymorphisms within the promoter and exonic sequences of CYBA, the gene that encodes the p22(phox) subunit of NADPH oxidase, have been characterized in the context of cardiovascular diseases.
Some examples include the alanine-to-valine substitution at codon 222 (Ala222-->Val) [DNA: C-to-T substitution at nucleo-tide 677 (677C-->T)] in methylenetetrahydrofolate reductase (NADPH) and the cofactor FAD (in relation to cardiovascular disease, migraines, and rages), the Pro187-->Ser (DNA: 609C-->T) mutation in NAD(P):quinone oxidoreductase 1 [NAD(P)H dehy-drogenase (quinone)] and FAD (in relation to cancer), the Ala44-->Gly (DNA: 131C-->G) mutation in glucose-6-phosphate 1-dehydrogenase and NADP (in relation to favism and hemolytic anemia), and the Glu487-->Lys mutation (present in one-half of Asians) in aldehyde dehydrogenase (NAD + ) and NAD (in relation to alcohol intolerance, Alzheimer disease, and cancer).