Targeting lipidated amino acid deficiency mitigates fibrosis via a PPARα/CCL2 axis in metabolic dysfunction-associated steatohepatitis models.
Metabolic dysfunction-associated steatohepatitis (MASH) is rising globally despite recent therapeutic advances, highlighting the need to identify new targetable pathways. While dysregulated lipid and amino acid metabolism are established features of MASH, the interplay between these two metabolic pathways remains unexp...