ArticleNature communications2023
Cytoplasmic Endonuclease G promotes nonalcoholic fatty liver disease via mTORC2-AKT-ACLY and endoplasmic reticulum stress.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
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.
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.
Who cites it
26 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Gut microbiota-derived indole-3-propionic acid alleviates endoplasmic reticulum stress by regulating FMO2 in MASLD.Hepatology communications · 2026Article
- Single-Nucleotide Polymorphisms in Genes Associated with Mitochondrial and DNA Damage Response Modulate the Risk of Non-Alcoholic Fatty Liver Disease in Humans.International journal of molecular sciences · 2026Article
- Integrative Multi-Omics Mendelian Randomization Reveals Oxidative Stress Mechanisms in Major Depressive Disorder, Bipolar Disorder, and Schizophrenia.Antioxidants (Basel, Switzerland) · 2026Article
- mTOR in radiotherapy of lung cancer: Mechanisms of radiation resistance and therapeutic implications (Review).International journal of oncology · 2026Review
- Endonuclease G restores lipid homeostasis in spontaneously hypertensive rats: implications for mitochondrial function.Frontiers in physiology · 2026Article
- Inflammaging and osteoarthritis - therapeutic opportunities.Frontiers in immunology · 2026Review
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Review
- ARMH4 accelerates aging by maintaining a positive-feedback growth signaling circuit.Nature communications · 2025Article
- Exercise suppresses DEAF1 to normalize mTORC1 activity and reverse muscle aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exogenous hydrogen sulfide improves non-alcoholic fatty liver disease by inhibiting endoplasmic reticulum stress/NLRP3 inflammasome pathway.Molecular and cellular biochemistry · 2025Article
- Cannabinoid-2 receptor depletion promotes non-alcoholic fatty liver disease in mice via disturbing gut microbiota and tryptophan metabolism.Acta pharmacologica Sinica · 2025Article
- Divergent 3D genome organization in livers of cave and surface morphs ofbioRxiv : the preprint server for biology · 2025Article
- Impaired RelA signaling and lipid metabolism dysregulation in hepatocytes: driving forces in the progression of metabolic dysfunction-associated steatotic liver disease.Cell death discovery · 2025Article
- Aflatoxin B1-Induced Apoptosis in Donkey Kidney via EndoG-Mediated Endoplasmic Reticulum Stress.Veterinary sciences · 2025Article
- Endonuclease G promotes hepatic mitochondrial respiration by selectively increasing mitochondrial tRNAProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring drug repurposing as a therapeutic strategy for non-alcoholic fatty liver disease (NAFLD): identification of potential targets and pathways.Gastroenterology and hepatology from bed to bench · 2025Article
- The role of everolimus in malignant bone tumor therapy: Molecular mechanisms, preclinical evidence, and advances in clinical applications.Oncology reviews · 2025Review
- Multi-Omics Analysis and Validation of Cell Senescence-Related Genes Associated with Non-Alcoholic Fatty Liver Disease.Journal of inflammation research · 2025Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endonuclease G (ENDOG), a nuclear-encoded mitochondrial intermembrane space protein, is well known to be translocated into the nucleus during apoptosis. Recent studies have shown that ENDOG might enter the mitochondrial matrix to regulate mitochondrial genome cleavage and replication. However, little is known about the role of ENDOG in the cytosol. Our previous work showed that cytoplasmic ENDOG competitively binds with 14-3-3γ, which released TSC2 to repress mTORC1 signaling and induce autophagy. Here, we demonstrate that cytoplasmic ENDOG could also release Rictor from 14-3-3γ to activate the mTORC2-AKT-ACLY axis, resulting in acetyl-CoA production. Importantly, we observe that ENDOG could translocate to the ER, bind with Bip, and release IRE1a/PERK to activate the endoplasmic reticulum stress response, promoting lipid synthesis. Taken together, we demonstrate that loss of ENDOG suppresses acetyl-CoA production and lipid synthesis, along with reducing endoplasmic reticulum stress, which eventually alleviates high-fat diet-induced nonalcoholic fatty liver disease in female mice.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.