ArticleMolecular medicine reports2021
Cigarette smoke extract stimulates PCSK9 production in HepG2 cells via ROS/NF‑κB signaling.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Selenium-Astaxanthin Co-Supplementation Synergistically Reduces PCSK9 Expression, Upregulates LDL Receptors, and Improves lipid profile and Cardiovascular Markers in Menopausal Ovariectomized Rats by attenuating inflammation and lipid peroxidation.Biological trace element research · 2026Article
- Association Between HNP1-3 and Atherosclerotic Plaque Burden in Subclinical Atherosclerosis and the Mediating Effect of PCSK9.Clinical and translational science · 2025Article
- Circulating Protein Mediators Linking Genetically Predicted Smoking to Abdominal Aortic Aneurysm: A Genomic-Proteomic Analysis.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Identifying Circulating Protein Mediators in the Link Between Smoking and Abdominal Aortic Aneurysm: An Integrated Analysis of Human Proteomic and Genomic Data.medRxiv : the preprint server for health sciences · 2025Article
- Isolation of highly polar galloyl glucoside tautomers from Saxifraga tangutica through preparative chromatography and assessment of their in vitro antioxidant activity.BMC chemistry · 2024Article
- Whole-Genome Resequencing Analysis of theInternational journal of molecular sciences · 2024Article
- The effect of smoking on tumor immunoediting: Friend or foe?Tobacco induced diseases · 2024Review
- Melatonin attenuates high glucose‑induced endothelial cell pyroptosis by activating the Nrf2 pathway to inhibit NLRP3 inflammasome activation.Molecular medicine reports · 2023Article
- IL-1β knockdown inhibits cigarette smoke extract-induced inflammation and apoptosis in vascular smooth muscle cells.PloS one · 2023Article
- Curcumin activates autophagy and attenuates high glucose-induced apoptosis in HUVECs through the ROS/NF-κB signaling pathway.Experimental and therapeutic medicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoke (CS) exposure is a risk factor for dyslipidemia and atherosclerosis. Reduced expression of low‑density lipoprotein receptor (LDLR) in hepatocytes may be one of the underlying mechanisms for these disorders. The aim of the present study was to investigate the molecular mechanism underlying the regulatory effect of CS extract (CSE) on proprotein convertase subtilisin/kexin type 9 (PCSK9) and low LDLR expression in HepG2 cells. PCSK9 and LDLR mRNA and protein expression levels in HepG2 cells were evaluated after CSE treatment via reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. In addition, total intracellular reactive oxygen species (ROS) production was determined via 2,7‑dichlorofluorescein diacetate fluorescence. CSE significantly increased PCSK9 expression and inhibited LDLR expression in a time‑ and concentration‑dependent manner. Furthermore, CSE significantly induced ROS production and nuclear factor κB (NF‑κB) activation. However, pretreatment with a ROS scavenger or an NF‑κB inhibitor significantly attenuated the CSE‑induced changes in PCSK9 and LDLR expression. In addition, pretreatment with melatonin markedly reduced ROS production, NF‑κB activation and PCSK9 expression, and increased LDLR expression in the CSE‑treated cells. These data suggest that melatonin inhibits CSE‑regulated PCSK9 and LDLR production in HepG2 cells via ROS/NF‑κB signaling.
Indexed as
Identifiers
What OpenQuestion holds
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.