Scientists at UT Southwestern Medical Center report they have identified a protein, HELZ2, that acts as a key regulator of how many cholesterol-carrying particles the liver releases into the bloodstream by affecting the gene APOB. The study was published in the American Heart Association journal Circulation and could inform future research into heart disease and fatty liver disease.
Researchers at UT Southwestern Medical Center say they have identified a protein, HELZ2, that helps regulate how many cholesterol-carrying particles the liver releases into the bloodstream.
The study, published in the American Heart Association journal Circulation, focused on how HELZ2 influences apolipoprotein B (APOB), a gene required to produce apoB proteins. ApoB is a core component of lipoproteins—particles that transport cholesterol and fats through the blood.
The researchers found that HELZ2 can shorten the lifespan of APOB messenger RNA (mRNA) in liver cells. With the APOB message breaking down more quickly, cells produce less apoB protein, which in turn means fewer lipoprotein particles are released into circulation.
"These particles are a major driver of plaque buildup in the arteries," said senior author Zhao Zhang, an assistant professor at UT Southwestern. "What we found is that HELZ2 acts as a powerful control point for how many cholesterol-carrying particles ultimately enter the bloodstream."
The ScienceDaily release describing the work also reports that, in mouse studies, increased HELZ2 activity was linked to fewer circulating lipoproteins, including LDL (low-density lipoprotein) cholesterol and triglycerides, along with greater protection against atherosclerosis—while also being associated with increased fat accumulation in the liver.
