Evidence map›Paper›PMID 41255220›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

CIDEC Restricts Liver Regeneration by Disturbing Lipid Droplet Triglyceride Turnover.

Feng Ouyang, Yining Li, Zixuan Zhang, Fangfang Sun, Yihong Shi, Qian Gui, Da Luo, Changyong Hu, Hang Su, Kaiqi Shen and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. CIDEC Restricts Liver Regeneration by Disturbing Lipid Droplet Triglyceride Turnover.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Feng OuyangShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Yining LiShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Zixuan ZhangShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Fangfang SunShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Yihong ShiShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Qian GuiShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Da LuoShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Changyong HuShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Hang SuShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Kaiqi ShenShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Lu GaoShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Hui YangShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Feng-Jung ChenShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Rong LiMinistry of Education Key Laboratory of Metabolism and Molecular Medicine, Department of Endocrinology and Metabolism, Shanghai Key Laboratory of Lung Inflammation and Injury,Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Tong-Jin ZhaoShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Peng LiShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.
Tian-Shu YangShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, 200438, China.ORCID https://orcid.org/0000-0002-0772-9123

Funding

National Key Research and Development Program of China 2021YFA0804801National Key Research and Development Program of China 2024YFA1802800National Natural Science Foundation of China 32270724National Natural Science Foundation of China 32271334National Natural Science Foundation of China 32271517National Natural Science Foundation of China 32300956National Natural Science Foundation of China 32571487National Natural Science Foundation of China 92357302Shanghai Basic Research Field Project "Science and Technology Innovation Action Plan" 21JC1400400
6 · The paper itself

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 FAO inhibition, underscoring the central role of TG catabolism. Conversely, overexpression of CIDEC or the TG biosynthetic enzyme Diacylglycerol O-acyltransferase 2 (DGAT2) exacerbates TG retention and impairs liver regeneration. Notably, CIDEC depletion significantly improves regenerative outcomes in mice with chronic steatosis. These findings reveal a previously unrecognized role for LD fusion in regulating the TG storage-utilization balance, where its suppression promotes metabolic flexibility to meet the energetic demands of liver regeneration. This metabolic checkpoint may be targeted to overcome impaired liver regeneration associated with fatty liver disease.

Indexed as

Lipid DropletsLiver RegenerationTriglyceridesAnimalsDiacylglycerol O-AcyltransferaseFatty LiverHepatocytesHumansLipid MetabolismLiverMaleMiceMice, Inbred C57BLDiacylglycerol O-AcyltransferaseTriglyceridesCIDEClipid dropletliver regenerationtriglyceride

Identifiers

PMID41255220
PMCPMC12806313

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.