ArticleNature communications2019
Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- TMED family genes and their roles in human diseases.International journal of medical sciences · 2023Pooled it
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- Time-Restricted Feeding Alters Behavior in a Sex-Specific Manner in Mice With Neuropathic Pain.Molecular nutrition & food research · 2026Article
- SDF2L1 modulates oxLDL-induced endoplasmic reticulum stress, protein aggregation, and O-mannosylation in myocardial infarction and lung cancer.Cellular and molecular life sciences : CMLS · 2026Article
- In vivo CRISPR/Cas9 screens identify new regulators of B cell activation and plasma cell differentiation.The Journal of experimental medicine · 2026Article
- Feeding-regulated glycogen metabolism drives rhythmic liver protein secretion.Nature metabolism · 2026Article
- Single-Cell-Derived Malignant Epithelial Programs Define Prognostic Risk and Therapeutic Vulnerability in Ovarian Cancer.Journal of Cancer · 2026Article
- Marine-Derived Compounds: A New Horizon in Cancer, Renal, and Metabolic Disease Therapeutics.Marine drugs · 2025Review
- Identifying Pyroptosis-Hub Genes and Inflammation Cell Type-Related Genes in Ischemic Stroke.Molecular neurobiology · 2025Article
- Loss of ATG7 in microglia impairs UPR, triggers ferroptosis, and weakens amyloid pathology control.The Journal of experimental medicine · 2025Article
- UBE2J1 is identified as a novel plasma cell-related gene involved in the prognosis of high-grade serous ovarian cancer.Journal of translational medicine · 2025Article
- Dasatinib and Quercetin as Senolytic Drugs Improve Fat Deposition and Exhibit Antifibrotic Effects in the Medaka Metabolic Dysfunction-Associated Steatotic Liver Disease Model.Diseases (Basel, Switzerland) · 2024Article
- Quantitative proteomics reveals the mechanism of endoplasmic reticulum stress-mediated pulmonary fibrosis in mice.Heliyon · 2024Article
- Rethinking Diabetes from the Perspective of Diverse Insulin Actions in Various Organs.JMA journal · 2024Review
- Supervised discovery of interpretable gene programs from single-cell data.Nature biotechnology · 2024Article
- The circadian clock in the choroid plexus drives rhythms in multiple cellular processes under the control of the suprachiasmatic nucleus.Fluids and barriers of the CNS · 2024Article
- Glycomacropeptide as an Efficient Agent to Fight Pathophysiological Mechanisms of Metabolic Syndrome.Nutrients · 2024Article
- The Role ofInsects · 2024Article
- Identification of a natural PLA2 inhibitor from the marine fungusActa pharmaceutica Sinica. B · 2024Article
- Exploring mechanisms underlying diabetes comorbidities and strategies to prevent vascular complications.Diabetology international · 2024Review
Corrections and comments
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Authors and funding
25 authors at 11 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dynamic metabolic changes occur in the liver during the transition between fasting and feeding. Here we show that transient ER stress responses in the liver following feeding terminated by Sdf2l1 are essential for normal glucose and lipid homeostasis. Sdf2l1 regulates ERAD through interaction with a trafficking protein, TMED10. Suppression of Sdf2l1 expression in the liver results in insulin resistance and increases triglyceride content with sustained ER stress. In obese and diabetic mice, Sdf2l1 is downregulated due to decreased levels of nuclear XBP-1s, whereas restoration of Sdf2l1 expression ameliorates glucose intolerance and fatty liver with decreased ER stress. In diabetic patients, insufficient induction of Sdf2l1 correlates with progression of insulin resistance and steatohepatitis. Therefore, failure to build an ER stress response in the liver may be a causal factor in obesity-related diabetes and nonalcoholic steatohepatitis, for which Sdf2l1 could serve as a therapeutic target and sensitive biomarker.
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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 OpenQuestion graph.