Nonalcoholic fatty liver disease (NAFLD) is associated with increased cardiovascular risk, preclinical atherosclerotic damage, and vascular events due to insulin resistance and oxidative stress.
Do current and developing NAFLD therapies impact cardiovascular outcomes in subjects with NAFLD?
NAFLD is closely connected to increased cardiovascular risk through pathophysiological mechanisms like insulin resistance and oxidative stress, highlighting the potential cardiovascular impact of NAFLD therapies.
Evidence suggests a close connection between Nonalcoholic Fatty Liver Disease (NAFLD) and increased cardiovascular (CV) risk. Several cross-sectional studies report that NAFLD is related to preclinical atherosclerotic damage, and to coronary, cerebral and peripheral vascular events. Similar results have been showed by prospective studies and also by meta-analyzes on observational studies. The pathophysiological mechanisms of NAFLD are related to insulin resistance, which causes a dysfunction in adipokine production, especially adiponectin, from adipose tissue. A proinflammatory state and an increase in oxidative stress, due to increased reacting oxygen species (ROS) formation with consequent oxidation of free fatty acids and increased de novo lipogenesis with accumulation of triglycerides, are observed. These mechanisms may have an impact on atherosclerotic plaque formation and progression, and they can lead to increased cardiovascular risk in subjects with NAFLD. This review extensively discusses and comments current and developing NAFLD therapies and their possible impact on cardiovascular outcome.
Galiero et al. (Fri,) conducted a review in Nonalcoholic fatty liver disease (NAFLD) and cardiovascular disease. Nonalcoholic fatty liver disease (NAFLD) was evaluated. Nonalcoholic fatty liver disease (NAFLD) is associated with increased cardiovascular risk, preclinical atherosclerotic damage, and vascular events due to insulin resistance and oxidative stress.
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