{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ouyang F"],"funding":["National Natural Science Foundation of China","Shanghai Basic Research Field Project \"Science and Technology Innovation Action Plan\"","National Key Research and Development Program of China"],"pagination":["e07048"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12806313"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(3)"],"pubmed_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"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["CIDEC Restricts Liver Regeneration by Disturbing Lipid Droplet Triglyceride Turnover."],"pmcid":["PMC12806313"],"funding_grant_id":["21JC1400400","32571487","32300956","32271334","2021YFA0804801","2024YFA1802800","32271517","32270724","92357302"],"pubmed_authors":["Yang H","Shen K","Zhao TJ","Li P","Li R","Su H","Chen FJ","Shi Y","Luo D","Yang TS","Li Y","Hu C","Gui Q","Zhang Z","Ouyang F","Gao L","Sun F"],"additional_accession":[]},"is_claimable":false,"name":"CIDEC Restricts Liver Regeneration by Disturbing Lipid Droplet Triglyceride Turnover.","description":"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","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-06T15:07:47.236Z","creation":"2026-06-01T03:10:43.682Z"},"accession":"S-EPMC12806313","cross_references":{"pubmed":["41255220"],"doi":["10.1002/advs.202507048"]}}