ArticlePloS one2016
Nicotinate-Curcumin Impedes Foam Cell Formation from THP-1 Cells through Restoring Autophagy Flux.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 3 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 3 syntheses or guidelines pooled it, 59 citations in OpenAlex.
- Macrophage-associated kinase signaling in atherosclerosis - a systematic review.Cell communication and signaling : CCS · 2026Pooled it
- Exploring global research trends in Chinese medicine for atherosclerosis: a bibliometric study 2012-2023.Frontiers in cardiovascular medicine · 2024Pooled it
- Pooled it
- Effects of β‑hydroxybutyrate on restoring autophagic flux and mitochondrial function in macrophages exposed to oxidized low‑density lipoprotein.Molecular medicine reports · 2026Article
- The Marine-Derived Cyclopentapeptide Turnagainolide B Suppresses Melanoma via Autophagic Flux Disruption and Inhibits Tumorigenesis In Vivo.Marine drugs · 2026Article
- Alleviation of nonalcoholic steatohepatitis induced by tetracycline in rats by Coffee Arabica extract through autophagy signals (mTOR/LC3-B).Scientific reports · 2026Article
- Foam Cells: The Origin of Formation and Target for Plant-derived Bioactive Compounds.Current medicinal chemistry · 2026Review
- Nanostructured Delivery Systems for Curcumin: Improving Bioavailability and Plaque-Targeting Efficacy in Atherosclerosis.Pharmaceutics · 2025Review
- Antiatherogenic and Cardioprotective Effects of a Xanthine Derivative KMUP-1 in ApoE Knockout Mice.Cardiovascular therapeutics · 2025Article
- Application of Photodynamic Therapy in Cardiology.International journal of molecular sciences · 2024Review
- Natural compounds from botanical drugs targeting mTOR signaling pathway as promising therapeutics for atherosclerosis: A review.Frontiers in pharmacology · 2023Review
- KLF2 alleviates endothelial cell injury and inhibits the formation of THP‑1 macrophage‑derived foam cells by activating Nrf2 and enhancing autophagy.Experimental and therapeutic medicine · 2022Article
- The Impact of Oxidative Stress and AKT Pathway on Cancer Cell Functions and Its Application to Natural Products.Antioxidants (Basel, Switzerland) · 2022Review
- Putative therapeutic impacts of cardiac CTRP9 in ischaemia/reperfusion injury.Journal of cellular and molecular medicine · 2022Review
- Autophagy and Diabetic Encephalopathy: Mechanistic Insights and Potential Therapeutic Implications.Aging and disease · 2022Review
- Bioactive components to inhibit foam cell formation in atherosclerosis.Molecular biology reports · 2022Review
- Polyphenols: Chemoprevention and therapeutic potentials in hematological malignancies.Frontiers in nutrition · 2022Review
- Nicotinate-curcumin inhibits AngII-induced vascular smooth muscle cell phenotype switching by upregulating Daxx expression.Cell adhesion & migration · 2021Article
- Curcumin-mediated Photodynamic Therapy Inhibits the Phenotypic Transformation, Migration, and Foaming of Oxidized Low-density Lipoprotein-treated Vascular Smooth Muscle Cells by Promoting Autophagy.Journal of cardiovascular pharmacology · 2021Article
- Curcumin promotes functional recovery and inhibits neuronal apoptosis after spinal cord injury through the modulation of autophagy.The journal of spinal cord medicine · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous studies have indicated that a novel curcumin derivate nicotinate-curcumin (NC) has beneficial effects on the prevention of atherosclerosis, but the precise mechanisms are not fully understood. Given that autophagy regulates lipid metabolism, the present study was designed to investigate whether NC decreases foam cell formation through restoring autophagy flux in oxidized low-density lipoprotein (ox-LDL)-treated THP-1 cells. Our results showed that ox-LDL (100 μg/ml) was accumulated in THP-1 cells and impaired autophagy flux. Ox-LDL-induced impairment of autophagy was enhanced by treatment with the autophagy inhibitor chloroquine (CQ) and rescued by the autophagy inducer rapamycin. The aggregation of ox-LDL was increased by CQ, but decreased by rapamycin. In addition, colocalization of lipid droplets with LC3-II was remarkably reduced in ox-LDL group. In contrast, NC (10 μM) rescued the impaired autophagy flux by significantly increasing level of LC3-II, the number of autophagolysosomes, and the degradation of p62 in ox-LDL-treated THP-1 cells. Inhibition of the PI3K-Akt-mTOR signaling was required for NC-rescued autophagy flux. Notably, our results showed that NC remarkably promoted the colocalization of lipid droplets with autophagolysosomes, increased efflux of cholesterol, and reduced ox-LDL accumulation in THP-1 cells. However, treatment with 3-methyladenine (3-MA) or CQ reduced the protective effects of NC on lipid accumulation. Collectively, the findings suggest that NC decreases lipid accumulation in THP-1 cells through restoring autophagy flux, and further implicate that NC may be a potential therapeutic reagent to reverse atherosclerosis.
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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.