ArticleCell stress & chaperones2017
FOXO1 and LXRα downregulate the apolipoprotein A-I gene expression during hydrogen peroxide-induced oxidative stress in HepG2 cells.
Article in Cell stress & chaperones, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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Who cites it
4 citing papers in PubMed, 18 citations in OpenAlex.
- Biliary elimination of cholesterol can be modulated by hepatocyte mitochondrial Aquaporin-8 in mice.Scientific reports · 2026Article
- Association of genetic polymorphisms inPeerJ · 2019Article
- Tumor necrosis factor α stimulates endogenous apolipoprotein A-I expression and secretion by human monocytes and macrophages: role of MAP-kinases, NF-κB, and nuclear receptors PPARα and LXRs.Molecular and cellular biochemistry · 2018Article
- Diabetes and dyslipidemia: characterizing lipoprotein metabolism.Diabetes, metabolic syndrome and obesity : targets and therapy · 2017Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
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Abstract
Reactive oxygen species damage various cell components including DNA, proteins, and lipids, and these impairments could be a reason for severe human diseases including atherosclerosis. Forkhead box O1 (FOXO1), an important metabolic transcription factor, upregulates antioxidant and proapoptotic genes during oxidative stress. Apolipoprotein A-I (ApoA-I) forms high density lipoprotein (HDL) particles that are responsible for cholesterol transfer from peripheral tissues to liver for removal in bile in vertebrates. The main sources for plasma ApoA-I in mammals are liver and jejunum. Hepatic apoA-I transcription depends on a multitude of metabolic transcription factors. We demonstrate that ApoA-I synthesis and secretion are decreased during H
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