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CIDEC Restricts Liver Regeneration by Disturbing Lipid Droplet Triglyceride Turnover
Feng Ouyang1, Yining Li1, Zixuan Zhang1
1Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|November 19, 2025
Summary
Cell death-inducing DNA fragmentation factor-like Effector C (CIDEC) sequesters triglycerides, hindering liver regeneration. Depleting CIDEC mobilizes lipids, enhancing regeneration, especially in fatty liver disease.
Area of Science:
- Hepatology
- Molecular Biology
- Metabolic Regulation
Background:
- Liver regeneration requires precise lipid metabolism.
- Lipid droplet (LD) accumulation and fusion are key but poorly understood processes.
- The role of LD fusion proteins in lipid mobilization during regeneration is unclear.
Purpose of the Study:
- Investigate the role of LD-associated proteins in triglyceride mobilization during liver regeneration.
- Identify key regulators of lipid droplet dynamics impacting regenerative capacity.
- Explore therapeutic targets for impaired liver regeneration in fatty liver disease.
Main Methods:
- Integrated lipidomic and transcriptomic analyses in hepatocytes.
- Manipulation of Cell death-inducing DNA fragmentation factor-like Effector C (CIDEC) and Diacylglycerol O-acyltransferase 2 (DGAT2) expression.
- Assessment of liver regeneration and fatty acid oxidation in mouse models, including those with chronic steatosis.
Main Results:
- CIDEC identified as a negative regulator of liver regeneration by sequestering triglycerides within LDs.
- CIDEC depletion enhances triglyceride mobilization and fatty acid oxidation (FAO)-driven regeneration.
- Overexpression of CIDEC or DGAT2 impairs regeneration; CIDEC depletion improves outcomes in steatotic mice.
Conclusions:
- CIDEC acts as a metabolic gatekeeper, suppressing lipid mobilization and regeneration.
- Suppression of LD fusion by CIDEC inhibition promotes metabolic flexibility for regeneration.
- Targeting CIDEC may offer a strategy to improve liver regeneration in fatty liver disease.
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