CIDEC Restricts Liver Regeneration by Disturbing Lipid Droplet Triglyceride Turnover.

ABSTRACT: The transient accumulation of triglyceride (TG)-enriched lipid droplets (LDs) in hepatocytes during early liver regeneration is critical for generation but remains mechanistically unclear, particularly the roles of LD fusion-associated proteins in lipid mobilization. Here, through integrated lipidomic and transcriptomic analyses, Cell death-inducing DNA fragmentation factor-like Effector C (CIDEC), an LD-associated protein upregulated during this phase is identified, as a negative regulator of regeneration through its unexpected role in sequestering TG within LDs. Mechanistically, CIDEC acts as a metabolic gatekeeper: its depletion after peak LD accumulation promotes TG mobilization and enhances fatty acid oxidation (FAO)-driven regeneration. This pro-regenerative effect is abolished by FA

SUBMITTER: Ouyang F 

PROVIDER: S-EPMC12806313 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature