REV-ERB can reduce LDL (LDL) cholesterol in animal models

A paper published in Biochemical Pharmacology by researchers at Saint Louis University have studied through recombinant human proteins about how nuclear receptors called REV-ERB are involved in the regulation of cholesterol metabolism. Their findings suggest that drugs targeting such nuclear receptors may be able to reduce LDL (LDL) cholesterol in animal models.

Dr. Thomas Burris, Ph.D., director of pharmacology and physiology at the University of St. Louis, said that studying the nuclear receptor signaling, the intracellular information system is the basis of many physiological processes used by the body. He identifies the natural hormones that regulate the nuclear receptors, and then synthesizes the compounds to target these receptors to develop drugs that treat the disease. REV-ERB is a nuclear receptor, a protein that plays a variety of roles. In the past, Burris has studied its role in regulating the internal clock of mammals.

Cholesterol is an essential component of the cell membrane. Atherosclerosis, plaque accumulation in the arteries, is caused by cholesterol metabolism disorders. Drugs such as statins can reduce low-density lipoprotein (LDL) cholesterol levels and atherosclerosis risk, but they are not suitable for everyone. Some patients stop medication because of side effects. Thus, additional cholesterol-lowering drugs are required. Nuclear receptors regulate basic physiological processes such as growth, development and metabolic balance in vivo. REV-ERB is a nuclear receptor that binds to a particular DNA sequence and limits the transcription of the target gene. Studies over the past decade have shown that REV-ERB plays an important role in metabolic pathways. Previous data indicate that REV-ERB lacks lipid metabolism that results in destruction; mice lacking REV-ERB expression show a significant increase in LDL and total cholesterol.

Similarly, in the previous study, Burris found a recombinant version of SR9009 called REV-ERB to reduce cytoplasmic cholesterol and triglyceride levels in animal models. In this study, Burris found that REV-ERB worked in the inhibition of several cholesterol-related enzyme genes and that pharmacological activation of REV-ERB resulted in further inhibition of these genes, which was associated with reduced cholesterol levels. These results reveal the way REV-ERB directly and indirectly regulates cholesterol and indicates that targeted REV-ERB may be an effective method for clinically suppressing LDL cholesterol levels. Flarebio offers high-quality recombinant proteins like recombinant CDH15.