UT Southwestern scientists identify HELZ2 as liver master switch for cholesterol release, opening upstream alternative to statins; gain-of-function mutation in mice cut LDL, triglycerides, and fatty liver. Senior author Zhao Zhang. Published in AHA journal Circulation (2026;153(6):415). Sources: UT Southwestern Newsroom, ScienceDaily, MedicalXpress, SciTechDaily, Newswise, Mega Doctor News, Mirage News, Circulation.
A new study finds a liver protein called HELZ2 acts as a master switch for cholesterol release. Researchers at UT Southwestern Medical Center say boosting it could lead to a treatment that works upstream of every existing statin.
Researchers at UT Southwestern Medical Center identified HELZ2, a liver protein that controls how stable apolipoprotein B mRNA is inside liver cells. When HELZ2 activity rises, the liver makes fewer cholesterol-carrying lipoproteins. Mice with a gain-of-function mutation that boosted HELZ2 had lower LDL, lower triglycerides, and less fatty liver. The work, led by Zhao Zhang, appears in Circulation.
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