Our study uncovers a novel therapeutic axis in MASLD, in which PE enhances the stability of PPARα mRNA by directly binding to HNRNPA1, and consequently upregulates fatty acid β-oxidation. These findings not only position PE as a promising therapeutic candidate for MASLD but also identify the HNRNPA1-PPARα regulatory pathway as a potential mechanistic target for treating metabolic liver diseases.
Zhou et al. (Fri,) studied this question.