ArticleThe American journal of pathology2018
Impaired Fasting-Induced Adaptive Lipid Droplet Biogenesis in Liver-Specific Atg5-Deficient Mouse Liver Is Mediated by Persistent Nuclear Factor-Like 2 Activation.
Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 58 citations in OpenAlex.
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- Overlapping Yet Distinct Functions of Vacuole Membrane Protein 1 and Transmembrane Protein 41B in Modulating Hepatic Lipoprotein Secretion and Autophagy.Cellular and molecular gastroenterology and hepatology · 2026Article
- Protein quality control and antigen presentation in the development of hepatitis B-related hepatocellular carcinoma.Frontiers in pharmacology · 2026Review
- Adipose cullin 3 mediates the antiobesity effect of pan neddylation inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Therapeutic Potential ofFood science & nutrition · 2025Article
- Liver Metabolism at the Crossroads: The Reciprocal Control of Nutrient-Sensing Nuclear Receptors and Autophagy.International journal of molecular sciences · 2025Review
- Ceramide homeostasis in hepatic lipid droplets.Biochemical Society transactions · 2025Review
- Autophagy related 14 protects against liver injury by inhibiting multiple cell death pathways.eGastroenterology · 2025Article
- TIGAR exacerbates obesity by triggering LRRK2-mediated defects in macroautophagy and chaperone-mediated autophagy in adipocytes.Autophagy · 2024Article
- SPRED2 Is a Novel Regulator of Autophagy in Hepatocellular Carcinoma Cells and Normal Hepatocytes.International journal of molecular sciences · 2024Article
- Cullin 3 RING E3 ligase inactivation causes NRF2-dependent NADH reductive stress, hepatic lipodystrophy, and systemic insulin resistance.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Dysfunction of autophagy in high-fat diet-induced non-alcoholic fatty liver disease.Autophagy · 2024Review
- Lipid metabolism dynamics in cancer stem cells: potential targets for cancers.Frontiers in pharmacology · 2024Review
- Molecular Modulators and Receptors of Selective Autophagy: Disease Implication and Identification Strategies.International journal of biological sciences · 2024Review
- Interplay of energy metabolism and autophagy.Autophagy · 2024Review
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- SQSTM1/p62 and Hepatic Mallory-Denk Body Formation in Alcohol-Associated Liver Disease.The American journal of pathology · 2023Review
- Liver HMGCS2 is critical in the maintenance of liver lipid homeostasis during fasting.Genes & diseases · 2023Article
- Where is the field of autophagy research heading?Autophagy · 2023Article
- Lack of hepatic autophagy promotes severity of liver injury but not steatosis.Journal of hepatology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Lipid droplets (LDs) are intracellular organelles that store neutral lipids as energy reservoir. Recent studies suggest that autophagy is important in maintaining the homeostasis of intracellular LDs by either regulating the biogenesis of LDs, mobilization of fatty acids, or degradation of LDs in cultured cells. Increasing evidence also supports a role of autophagy in regulating glucose and lipid metabolism in vivo in mammals. In response to fasting/starvation, lipids are mobilized from the adipose tissue to the liver, which increases the number of intracellular LDs and stimulates fatty acid oxidation and ketogenesis. However, it is still controversial and unclear how impaired autophagy in hepatocytes affects the biogenesis of LDs in mouse livers. In the present study, it was demonstrated that hepatic autophagy-deficient (L-Atg)5 knockout mice had impaired adaptation to fasting-induced hepatic biogenesis of LDs. The maladaptation to fasting-induced hepatic biogenesis of LDs in L-Atg5 knockout mouse livers was not due to hepatic changes of de novo lipogenesis, secretion of very-low-density lipoprotein or fatty acid β-oxidation, but it was due to persistent nuclear factor-like 2 activation because biogenesis of LDs restored in L-Atg5/nuclear factor-like 2 double-knockout mice.
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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.