<i>PLIN5</i> deficiency ameliorates metabolic dysfunction‑associated fatty liver disease by inhibiting ferroptosis.

ABSTRACT: Metabolic‑associated fatty liver disease (MAFLD) is widely recognized as the most common type of chronic liver disease. As a member of the perilipin (PLIN) family, PLIN5 serves an important role in the regulation of lipid metabolism. Ferroptosis is a form of iron‑dependent non‑apoptotic cell death characterized by lipid peroxidation. Notably, knockout of PLIN5 can attenuate high‑fat diet (HFD)‑induced MAFLD; however, the specific underlying mechanism remains unclear. The present study induced PLIN5 overexpression by transfecting AML12 cells with a pcDNA3.1‑PLIN5 plasmid, and PLIN5 knockdown was achieved using short hairpin RNA‑mediated interference. Subsequently, intracellular ferrous iron (Fe²⁺) levels were assessed via immunofluorescence staining. F

SUBMITTER: Li Y 

PROVIDER: S-EPMC12555889 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature