ArticleThe EMBO journal2017
A postprandial FGF19-SHP-LSD1 regulatory axis mediates epigenetic repression of hepatic autophagy.
Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 66 citations in OpenAlex.
- The role of FGF19-FGFR4 signaling pathway in liver health and disease: Guardian or destroyer.Genes & diseases · 2026Review
- Nuclear class 3 PI3K co-activates fasting-specific chromatin remodelling.Nature cell biology · 2026Article
- Phosphorylation of OTUB1 promotes autophagy initiation under starvation.Nature communications · 2026Article
- Transcriptional and epigenetic regulation of autophagy: mechanisms, disease relevance and therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Aberrant miR-378 expression promotes hepatic lipid accumulation via hijacking the bile acid-regulated autophagy.Life metabolism · 2026Article
- Hepatocyte Autophagy in Malaria: Current Concepts, Emerging Mechanisms, and Future Therapeutic Directions.Pathogens (Basel, Switzerland) · 2026Review
- Autophagy in the liver.Autophagy reports · 2026Review
- FGF19 in Solid Tumors: Molecular Mechanisms, Metabolic Reprogramming, and Emerging Therapeutic Opportunities.Theranostics · 2026Review
- The role of fibroblast growth factors in cell and cancer metabolism.FEBS letters · 2026Review
- FGF-based drug discovery: advances and challenges.Nature reviews. Drug discovery · 2025Review
- Review
- Menin maintains lysosomal and mitochondrial homeostasis through epigenetic mechanisms in lung cancer.Cell death & disease · 2025Article
- Identification of chikusetsusaponin IVa as a novel lysine-specific demethylase 1 inhibitor that ameliorates high fat diet-induced MASLD in mice.Acta pharmacologica Sinica · 2025Article
- Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025Review
- Bile acids regulation of cellular stress responses in liver physiology and diseases.eGastroenterology · 2024Article
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- Advances in the molecular mechanism and targeted therapy of radioactive-iodine refractory differentiated thyroid cancer.Medical oncology (Northwood, London, England) · 2023Review
- Regulation of autophagy gene expression and its implications in cancer.Journal of cell science · 2023Review
- Transcriptional control of energy metabolism by nuclear receptors.Nature reviews. Molecular cell biology · 2022Review
- Feeding activates FGF15-SHP-TFEB-mediated lipophagy in the gut.The EMBO journal · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Lysosome-mediated autophagy is essential for cellular survival and homeostasis upon nutrient deprivation, but is repressed after feeding. Despite the emerging importance of transcriptional regulation of autophagy by nutrient-sensing factors, the role for epigenetic control is largely unexplored. Here, we show that Small Heterodimer Partner (SHP) mediates postprandial epigenetic repression of hepatic autophagy by recruiting histone demethylase LSD1 in response to a late fed-state hormone, FGF19 (hFGF19, mFGF15). FGF19 treatment or feeding inhibits macroautophagy, including lipophagy, but these effects are blunted in SHP-null mice or LSD1-depleted mice. In addition, feeding-mediated autophagy inhibition is attenuated in FGF15-null mice. Upon FGF19 treatment or feeding, SHP recruits LSD1 to CREB-bound autophagy genes, including Tfeb, resulting in dissociation of CRTC2, LSD1-mediated demethylation of gene-activation histone marks H3K4-me2/3, and subsequent accumulation of repressive histone modifications. Both FXR and SHP inhibit hepatic autophagy interdependently, but while FXR acts early, SHP acts relatively late after feeding, which effectively sustains postprandial inhibition of autophagy. This study demonstrates that the FGF19-SHP-LSD1 axis maintains homeostasis by suppressing unnecessary autophagic breakdown of cellular components, including lipids, under nutrient-rich postprandial conditions.
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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.