Table 1.
Condition | Involved mechanisms |
---|---|
Hypertension | Endothelial dysfunction, reduced NO, increased levels of endothelial growth factor, plasminogen-1 and thromboxane A2 increasing peripheral vascular resistance and arterial stiffness |
Atherosclerosis | Visceral obesity associated to a rapid progression of coronary calcifications and to a greater vulnerability of atherosclerotic plaques |
Heart failure | Neurohormonal imbalance, increased production of ROS, inflammatory mediators, leptin, resistin, visfatin and adipsin and reduced synthesis of adiponectin |
Diabetes | Activation of NF-κB, p38 and MAPK pathways, increased levels of IFN γ, TNFα, MCP-1, IL-1β and IL-6 and adipokines leading to insulin resistance and of concomitant metabolic alterations |
Venous thromboembolism | Elevated levels of prothrombotic molecules including Factor VII, fibrinogen and tissue factor and increased expression of plasminogen activator inhibitor-1 (PAI-1) |
Pulmonary hypertension | Elevated levels of cytokines, TNF-α, and interleukins, IFN γ, insulin resistance and oxidative stress |
See the text for abbreviations.