ArticleScientific reports2017
2-Hydroxypropyl-beta-cyclodextrin (HPβCD) reduces age-related lipofuscin accumulation through a cholesterol-associated pathway.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Cholesterol Drives IFITM3CNS neuroscience & therapeutics · 2026Article
- 2-Hydroxypropyl-β-cyclodextrin accesses acute and subacute infarcts in a mouse model of ischemic stroke.Fluids and barriers of the CNS · 2026Article
- Cyclodextrin-Based Formulations as a Promising Strategy to Overcome the Blood-Brain Barrier: Historical Overview and Prospects in Glioblastoma Treatment.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Effects of Target of Rapamycin and Phosphatidylinositol 3-Kinase Inhibitors and Other Autophagy-Related Supplements on Life Span inInternational journal of molecular sciences · 2024Article
- 2-Hydroxypropyl-β-cyclodextrin (HPβCD) as a Potential Therapeutic Agent for Breast Cancer.Cancers · 2023Article
- Repeated Administration of 2-Hydroxypropyl-β-Cyclodextrin (HPβCD) Attenuates the Chronic Inflammatory Response to Experimental Stroke.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Article
- A newly characterized exopolysaccharide from Sanghuangporus sanghuang.Journal of microbiology (Seoul, Korea) · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress causes significant increases in both cholesterol uptake and intracellular accumulation of the aging biomarker lipofuscin. Here we show that HPβCD addition mitigates these adverse effects in human fibroblasts by significantly reducing LDLr and SREBP1 gene expression. In the absence of oxidative stress, HPβCD addition induces a paradoxical response, increasing cholesterol accumulation (but not lipofuscin) via upregulation of cholesterol biosynthesis. These two distinct, but opposite effects highlight a previously overlooked therapeutic consideration: the cholesterol content of the treated cell determines which cholesterol pathways, either beneficial or harmful, are responsive to HPβCD.
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Registered trials
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