A new therapy that helps increase good cholesterol and lower triglycerides in the blood could be a potential tool for combating cardiovascular disease, US researchers say. The new therapy has been found effective in non-human primates. The study was conducted because there is a very strong inverse correlation between the amount of HDL (good cholesterol) and heart disease, said co-principal investigator Ryan Temel, Ph.D., an assistant professor of pathology and lipid sciences at Wake Forest Baptist. "The higher your level of HDL, the lower your risk of developing cardiovascular disease. Currently, however, there are few therapies that significantly raise HDL," he stated. While there are several effective therapies available on the market for lowering LDL, or bad cholesterol, modern medicine has yet to find a good way to raise HDL, Temel noted. He and colleagues from NYU Langone Medical Center and Regulus Therapeutics Inc., a biopharmaceutical company, are studying a new drug that targets microRNA-33 (miR-33). MiR-33 is a small RNA molecule that reduces HDL and increases triglyceride production. The researchers tested the drug, anti-miR-33, in non-human primates and found that it increased HDL cholesterol and lowered triglycerides. In the study, use of the drug resulted in a maximum HDL cholesterol increase of 50 percent after eight weeks that was sustained throughout the remainder of the 12-week study. Anti-miR-33a/b treatment in the non-human primate model also increased the expression of miR-33 target genes involved in fatty acid breakdown resulting in suppressed triglyceride levels, a finding not previously observed in mice. The decrease in triglycerides was apparent after four weeks and reached a maximum reduction of 50 per cent. These findings indicate that miR-33a and miR-33b are key regulators of cholesterol and fatty acid metabolism, Temel added, and that an anti-miR-33 approach could directly impact atherosclerosis, as well as address important cardiovascular risk factors such low HDL and high triglycerides.