ArticleThe Journal of biological chemistry
Loss of Down syndrome critical region-1 leads to cholesterol metabolic dysfunction that exaggerates hypercholesterolemia in ApoE-null background.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Lipoprotein(a) levels in Down syndrome: A conundrum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Prevalence and Risk Factors of Metabolic-Associated Fatty Liver Disease in Children with Down Syndrome at a Tertiary Care Center.Journal of clinical medicine · 2025Article
- Research progress on the correlation between corneal neovascularization and lymphangiogenesis (Review).Molecular medicine reports · 2025Review
- STRIDE-DB: a comprehensive database for exploration of instability and phenotypic relevance of short tandem repeats in the human genome.Database : the journal of biological databases and curation · 2024Article
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Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down syndrome critical region (DSCR)-1 functions as a feedback modulator for calcineurin-nuclear factor for activated T cell (NFAT) signals, which are crucial for cell proliferation and inflammation. Stable expression of DSCR-1 inhibits pathological angiogenesis and septic inflammation. DSCR-1 also plays a critical role in vascular wall remodeling associated with aneurysm development that occurs primarily in smooth muscle cells. Besides, Dscr-1 deficiency promotes the M1-to M2-like phenotypic switch in macrophages, which correlates to the reduction of denatured cholesterol uptakes. However, the distinct roles of DSCR-1 in cholesterol and lipid metabolism are not well understood. Here, we show that loss of apolipoprotein (Apo) E in mice with chronic hypercholesterolemia induced Dscr-1 expression in the liver and aortic atheroma. In Dscr-1-null mice fed a high-fat diet, oxidative- and endoplasmic reticulum (ER) stress was induced, and sterol regulatory element-binding protein (SREBP) 2 production in hepatocytes was stimulated. This exaggerated ApoE
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Registered trials
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