Researchers at UT Southwestern Medical Center have identified a protein that acts as a key regulator of how the liver releases cholesterol carrying particles into the bloodstream. The discovery could eventually lead to new treatments for heart disease and fatty liver disease.
The study, published in the American Heart Association journal Circulation, focused on a protein called HELZ2. Scientists found that HELZ2 helps control the activity of apolipoprotein B (APOB), a gene required to produce apoB proteins that form lipoproteins, the particles responsible for transporting cholesterol and fats through the body.
"These particles are a major driver of plaque buildup in the arteries," said senior author Zhao Zhang, Ph.D., Assistant Professor in UT Southwestern's Center for the Genetics of Host Defense and of Internal Medicine. "What we found is that HELZ2 acts as a powerful control point for how many cholesterol-carrying particles ultimately enter the bloodstream."
How HELZ2 Reduces Harmful Cholesterol
The team discovered that HELZ2 works by shortening the lifespan of APOB messenger RNA (mRNA) inside liver cells. Messenger RNA carries the instructions needed for cells to make proteins. When HELZ2 activity rises, the APOB message breaks down more quickly, resulting in lower production of apoB proteins and fewer cholesterol carrying lipoproteins entering the blood.
