ArticleCellular and molecular gastroenterology and hepatology2022
mTORC2 Facilitates Liver Regeneration Through Sphingolipid-Induced PPAR-α-Fatty Acid Oxidation.
Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- mTORC2 regulates lipid metabolism-driven TAMs via the PPAR-γ/CD36 pathway to promote liposarcoma progression.Adipocyte · 2026Article
- Endogenous phosphatidylcholine 16:0/20:4 increases to promote liver regeneration in hepatectomy.iScience · 2026Article
- Lentiviral-Mediated Expression of a Novel Transforming Growth Factor‑β (TGF-β) Inhibitor Peptibody Therapeutically Mitigates Established Liver Fibrosis by Modulating Inflammation and Inducing Metabolic Reprogramming.ACS pharmacology & translational science · 2026Article
- Therapeutic priming of liver regeneration: from mechanisms toFrontiers in transplantation · 2026Review
- Liver regeneration: unraveling the molecular mechanisms and clinical application.Journal of translational medicine · 2025Review
- Patient-derived colon epithelial organoids reveal lipid-related metabolic dysfunction in pediatric ulcerative colitis.Nature communications · 2025Article
- Lipid metabolism orchestrates liver regeneration: an integrated metabolic network.Journal of translational medicine · 2025Review
- A Perspective on the Role of Metformin in Treating Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Long COVID.ACS pharmacology & translational science · 2025Review
- Targeting mTORC2 in lung squamous cell carcinoma improves anti-tumor immunity through the PSGL-1-VISTA axis.Cancer gene therapy · 2025Article
- Modelling the liver's regenerative capacity across different clinical conditions.JHEP reports : innovation in hepatology · 2025Article
- Article
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Plasma GLP-1 and metabolic dynamics during human liver regeneration and their association with posthepatectomy liver failure.Hepatobiliary surgery and nutrition · 2025Article
- Vitamin D alleviates obesity-related metabolic abnormalities by modulating the gut microbiota in older female mice on a high-fat diet.Frontiers in cellular and infection microbiology · 2025Article
- Metabolic disturbances in acute pancreatitis: mechanisms and therapeutic implications.Frontiers in endocrinology · 2025Review
- Review
- Network-level analysis of ageing and its relationship with diseases and tissue regeneration in the mouse liver.Scientific reports · 2023Article
- ATL I, Acts as a SIRT6 Activator to Alleviate Hepatic Steatosis in Mice via Suppression of NLRP3 Inflammasome Formation.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Role of Steatosis in Preventing Post-hepatectomy Liver Failure After Major Resection: Findings From an Animal Study.Journal of clinical and experimental hepatologyArticle
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Authors and funding
19 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsDuring liver regeneration after partial hepatectomy, the function and metabolic pathways governing transient lipid droplet accumulation in hepatocytes remain obscure. Mammalian target of rapamycin 2 (mTORC2) facilitates de novo synthesis of hepatic lipids. Under normal conditions and in tumorigenesis, decreased levels of triglyceride (TG) and fatty acids (FAs) are observed in the mTORC2-deficient liver. However, during liver regeneration, their levels increase in the absence of mTORC2.
methodsRictor liver-specific knockout and control mice underwent partial hepatectomy, followed by measurement of TG and FA contents during liver regeneration. FA metabolism was evaluated by analyzing the expression of FA metabolism-related genes and proteins. Intraperitoneal injection of the peroxisome proliferator-activated receptor α (PPAR-α) agonist, p53 inhibitor, and protein kinase B (AKT) activator was performed to verify the regulatory pathways involved. Lipid mass spectrometry was performed to identify the potential PPAR-α activators.
resultsThe expression of FA metabolism-related genes and proteins suggested that FAs are mainly transported into hepatocytes during liver regeneration. The PPAR-α pathway is down-regulated significantly in the mTORC2-deficient liver, resulting in the accumulation of TGs. The PPAR-α agonist WY-14643 rescued deficient liver regeneration and survival in mTORC2-deficient mice. Furthermore, lipidomic analysis suggested that mTORC2 deficiency substantially reduced glucosylceramide (GluCer) content. GluCer activated PPAR-α. GluCer treatment in vivo restored the regenerative ability and survival rates in the mTORC2-deficient group.
conclusionsOur data suggest that FAs are mainly transported into hepatocytes during liver regeneration, and their metabolism is facilitated by mTORC2 through the GluCer-PPAR-α pathway, thereby establishing a novel role for mTORC2 in lipid metabolism.
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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.