New evidence for nicotinic acid treatment to reduce atherosclerosis

Abstract

Nicotinic acid (at a daily dose of grams) has been shown to induce potent antiatherosclerotic effects in human and animal models. Evidence from clinical studies performed in the 1950s has shown that nicotinic acid treatment remarkably improves the plasma lipid profile. Large clinical studies showed that nicotinic acid improves clinical cardiovascular outcomes. Given the protective effects of niacin, basic research studies were designed to explore additional antiatherosclerotic pathways, such as those involved in cardiovascular inflammation. After the discovery of the nicotinic acid receptor GPR109A on adipocytes and immune cells, novel direct immunomodulatory properties of nicotinic acid have been identified. Importantly, the regulation of the release of inflammatory mediators from adipose tissue was observed, independent of lipid level amelioration. Less is known about the possible direct anti-inflammatory activities of nicotinic acid in other cells (such as hepatocytes, endothelial and vascular cells) previously indicated as key players in atherogenesis. Thus, further studies are needed to clarify this promising topic. Emerging evidence from clinical and basic research studies indicates that novel direct antiatherosclerotic properties might mediate nicotinic acid-induced cardiovascular protection. Despite some limitations in its clinical use (mainly due to the incidence of adverse events, such as cutaneous flushing and hepatotoxicity), nicotinic acid should be considered as a very potent therapeutic approach to reduce atherosclerosis. Promising research developments are warranted in the near future.

Keywords::

• atherosclerosis
• cardiovascular risk
• cholesterol
• inflammation
• nicotinic acid

Financial & competing interests disclosure

This work was funded by the ‘Sir Jules Thorn Trust Reg’ fund and Prévot fund to Fabrizio Montecucco. This work was funded by EU FP7, Grant number 201668, AtheroRemo and supported by grants from the Swiss National Science Foundation (# 310030-118245), De Reuter Foundation and Boninchi Foundation to François Mach. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.