ArticleThe Journal of clinical investigation2016
Inhibition of apolipoprotein B synthesis stimulates endoplasmic reticulum autophagy that prevents steatosis.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
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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.
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Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- A humanized mouse model of APOB deficiency recapitulates hypobetalipoproteinemia.Journal of lipid research · 2026Article
- ER stress-mediated impairment of hepatic lipid export is associated with steatosis in AKI-induced remote liver injury.Scientific reports · 2026Article
- ER Stress-Mediated Impairment of Hepatic Lipid Export Drives Steatosis in AKI-Induced Remote Liver Injury.Research square · 2026Article
- Current and Emerging Issues in Familial Hypobetalipoproteinemia-related Steatotic Liver Diseases.Journal of clinical and translational hepatology · 2025Review
- The Framingham steatosis index as a predictor of advanced CKM syndrome in US adults: Evidence from NHANES 2001 to 2018.Medicine · 2025Article
- Human hepatoma Huh-7 cell culture models deficient in apolipoprotein B secretion.Journal of lipid research · 2025Article
- The Biology and Clinical Implications of PCSK7.Endocrine reviews · 2025Review
- Walking the VLDL tightrope in cardiometabolic diseases.Trends in endocrinology and metabolism: TEM · 2025Review
- Casz1 and Znf101/Zfp961 differentially regulate apolipoproteins A1 and B, alter plasma lipoproteins, and reduce atherosclerosis.JCI insight · 2025Article
- Two sides of the same coin: Non-alcoholic fatty liver disease and atherosclerosis.Vascular pharmacology · 2024Review
- Article
- VLDL Biogenesis and Secretion: It Takes a Village.Circulation research · 2024Review
- A pan-cancer analysis of the oncogenic and immunological roles of apolipoprotein F (APOF) in human cancer.European journal of medical research · 2023Article
- Surf4, cargo trafficking, lipid metabolism, and therapeutic implications.Journal of molecular cell biology · 2023Review
- Hepatocytes Deficient in Nuclear Envelope Protein Lamina-associated Polypeptide 1 are an Ideal Mammalian System to Study Intranuclear Lipid Droplets.Journal of lipid research · 2022Article
- Antisense oligonucleotide is a promising intervention for liver diseases.Frontiers in pharmacology · 2022Review
- Lipid droplet screen in human hepatocytes identifies TRRAP as a regulator of cellular triglyceride metabolism.Clinical and translational science · 2021Article
- Clodronate, an inhibitor of the vesicular nucleotide transporter, ameliorates steatohepatitis and acute liver injury.Scientific reports · 2021Article
- Review
- Simultaneous Inhibition of Peripheral CB1R and iNOS Mitigates Obesity-Related Dyslipidemia Through Distinct Mechanisms.Diabetes · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Inhibition of VLDL secretion reduces plasma levels of atherogenic apolipoprotein B (apoB) lipoproteins but can also cause hepatic steatosis. Approaches targeting apoB synthesis, which lies upstream of VLDL secretion, have potential to effectively reduce dyslipidemia but can also lead to hepatic accumulation of unsecreted triglycerides (TG). Here, we found that treating mice with apoB antisense oligonucleotides (ASOs) for 6 weeks decreased VLDL secretion and plasma cholesterol without causing steatosis. The absence of steatosis was linked to an increase in ER stress in the first 3 weeks of ASO treatment, followed by development of ER autophagy at the end of 6 weeks of treatment. The latter resulted in increased fatty acid (FA) oxidation that was inhibited by both chloroquine and 3-methyl adenine, consistent with trafficking of ER TG through the autophagic pathway before oxidation. These findings support the concept that inhibition of apoB synthesis traps lipids that have been transferred to the ER by microsomal TG transfer protein (MTP), inducing ER stress. ER stress then triggers ER autophagy and subsequent lysosomal lipolysis of TG, followed by mitochondrial oxidation of released FA, leading to prevention of steatosis. The identification of this pathway indicates that inhibition of VLDL secretion remains a viable target for therapies aiming to reduce circulating levels of atherogenic apoB lipoproteins.
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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.