Researchers found that inhibiting specific RNA molecules in the cells of mice boosted production of a protein that removes LDL cholesterol from the blood.
The results suggest therapies could be developed for humans, who share the same genes and proteins, to maintain cholesterol balance.
Researchers from New York University School of Medicine examined the cholesterol-regulating protein ABCA1, which works to increase HDL cholesterol and reduce LDL cholesterol in the blood.
They found that a microRNA molecule called miR-33 prevents cells from producing the cholesterol-reducing protein in mice.
However, the researchers also discovered that, when they blocked the function of the miRNAs in mice cells, it caused the production of the protein. This led to reduced LDL cholesterol levels in the body, as well as improved levels of HDL cholesterol. The authors said: 'Our data provides evidence for a role for miR-33 in the epigenetic regulation of cholesterol homeostasis.'
The authors concluded that blocking the function of miR-33 could yield potential treatment in humans. 'Our study suggests that antagonists of endogenous miR-33 may be a useful therapeutic strategy for enhancing ABCA1 expression and raising HDL levels in vivo.'