As there are a variety of CVDs and causes for CVD, there is no one specific mechanism that can cause CVD. However, there are general components shown to promote CVD development which can be found in a few pathways. Reactive Oxygen Species (ROS): ROS are produced through numerous processes in our cells, including the induction of oxidative enzymes. The notable species involved in human cells include superoxide anion (O2-), hydroxyl radicals (OH), and hydrogen peroxide (H2O2). Not only does ROS physiologically have a role in controlling the vasculature through tone and endothelial and cardiac function, but it also is a vital player in inflammation, promoting apoptosis, angiogenesis and much more. Additionally, ROS causes oxidative stress within the body which, although may not be the sole proprietor, exacerbates the various factors that contribute to developing CVD, especially hypertension. Finally, ROS also act as signaling molecules to induce the body’s inflammatory response to prevent any further damage from happening, which can lead to cell and tissue damage of the vasculature if not moderated appropriately. Induction of oxidative enzymes: Cytosolic oxidases are another critical component in ROS production. These enzymes transfer electrons to create radicals or superoxide, and increase oxidative stress. These enzymes have also shown to be present in various physiological stressful situations, which is associated with hypertension and other traditional risk factors negatively impacting CVD. * Xanthine oxidase (XO): XO, under normal circumstances, is an important enzyme in producing uric acid, released from the kidneys. These are typically located in the liver, however under times of stress from ROS, can increase its activity. This elevates vascular tone and even ROS production in the form of superoxide, thus contributing to higher oxidative stress. * Nitric oxide synthase: Nitric oxide synthases are known for producing nitric oxide, which has numerous functions in the body including vasodilation – i.e. widening of the vessels. Nitric oxide reacts with other forms of ROS to create potent oxidants, consequently causing other pathologic conditions, including heart failure and myocardial infarction. Moreover, this family of enzymes are crucial signaling molecules in regulating vascular tone and multiple other functions. Thus, any disruption in regular functioning impacts the vascular tone regulation. * NADH/NADPH oxidase: These enzymes contribute significantly to the amount of ROS present in the body. If in cardiac distress, an individual may induce excessive production, which may in turn lead to the pathogenesis of varying forms of tissue damage and cellular dysfunction in cardiac muscles. Uncoupling of Mitochondrial electron transport chain: The mitochondria is a contributor to the levels of ROS we see within our body. Not only does it produce it, but is also vulnerable to the damage caused by ROS. It also is a key player of cell function in the<unk>  system. With this damage to the mitochondria, the cell’s function may be altered as not enough energy is being produced as needed, thus hindering the cell’s ability to function optimally. These events create a disastrous feedback loop where further mitochondrial damage results in increased ROS production, which furthers the damage and contributes to the risk of developing CVD. Immune cell infiltration and cytokines: A large contributing risk factor to the development of CVD is the production of plaque, also known as atherogenesis or atherosclerosis. This condition is known to involve multiple inflammatory cascades from the immune system responding to varying pathogens. Elevated inflammatory cytokines, including interleukin-6 and tumor necrosis factor-⍺, initiate a cascade conducive to plaque production.
Cardiovascular disease in women
Thyroid disease in women
Risk factors for breast cancer
Autoimmune disease in women
Male lactation
High-risk pregnancy
Sleep problems in women
Women and smoking