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Abstract
Statins lower cholesterol and are commonly prescribed for prevention and treatment of cardiovascular disease risk. Statins have pleotropic actions beyond cholesterol lowering, including decreased protein prenylation, which can alter immune function. The general anti-inflammatory effect of statins may be a key pleiotropic effect that improves cardiovascular disease risk. However, a series of findings have shown that statins increase the pro-inflammatory cytokine, IL-1β, via decreased protein prenylation in immune cells. IL-1β can be regulated by the NLRP3 inflammasome containing caspase-1. Statins have been associated with an increased risk of new onset diabetes. Inflammation can promote ineffective insulin action (insulin resistance), which often precedes diabetes. This review highlights the links between statins, insulin resistance and immunity via the NLRP3 inflammasome. We propose that statin-induced changes in immunity should be investigated as a mechanism underlying increased risk of diabetes. It is possible that statin-related insulin resistance occurs through a separate pathway from various mechanisms that confer cardiovascular benefits. Therefore, understanding the potential mechanisms that segregate statin-induced cardiovascular effects from those that cause dysglycemia may lead to improvements in this drugs class.
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Funding
BDH was supported by an Ontario Graduate Scholarship (OGS). Supported by operating grants to JDS from the Canadian Institutes of Health Research (CIHR; MOP-130432) and the Canadian Diabetes Association (CDA; SC-5-12-3891-JS). JDS holds CDA Scholar (OG-3-12-3745-JS) and CIHR New Investigator awards (MSH-136665).