ArticleInternational journal of molecular sciences2019
Quercetin Suppresses the Progression of Atherosclerosis by Regulating MST1-Mediated Autophagy in ox-LDL-Induced RAW264.7 Macrophage Foam Cells.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 2 of them syntheses that pooled it.
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
100 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.
- Exploring global research trends in Chinese medicine for atherosclerosis: a bibliometric study 2012-2023.Frontiers in cardiovascular medicine · 2024Pooled it
- Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation.Frontiers in immunology · 2022Pooled it
- Nrf2 deficiency in myeloid cells accelerates atherosclerosis by promoting the inflammatory response and impairing efferocytosis.Journal of advanced research · 2026Article
- Freeze-DriedBiomolecules · 2026Article
- Identification of PRKCB, NLRC4, and TNFSF10 as Key Regulators of the Lipid Metabolism-Autophagy Network in Atherosclerosis.Cell biochemistry and function · 2026Article
- Tumor Microenvironment Hijacks and Accelerates a Physiological Myeloid Senescence Signature Associated with Pan-Cancer Immunosuppression and Prognostic Stratification.International journal of molecular sciences · 2026Article
- Mitophagy in Macrophages: A Metabolic Checkpoint in Inflammation-to-Repair Transition in Atherosclerosis.Journal of the American Heart Association · 2026Review
- Atherosclerotic Plaque Characterization Magnetic Resonance Imaging In Vitro at 1.5 Tesla for the Assessment of Coronary Artery Disease.Journal of clinical medicine · 2026Article
- Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review).International journal of molecular medicine · 2026Review
- Autophagy-mediated Kupffer cell polarization in liver cirrhosis reversal: Mechanistic insights and therapeutic strategies.Liver research (Beijing, China) · 2026Review
- Rapamycin Reduces Amyloid-β Plaques and Improves Behavioral Performance in a Sex-Dependent Manner in Mouse Models of Amyloidosis.CNS neuroscience & therapeutics · 2026Article
- Intestinal aging-related immune dysfunction: mechanisms and interventions.Acta biochimica et biophysica Sinica · 2026Review
- A bibliometric analysis of autophagy research in atherosclerosis over the past decade.Medicine · 2026Review
- Quercetin Promotes the M1-to-M2 Macrophage Phenotypic Switch During Liver Fibrosis Treatment by Modulating the JAK2/STAT3 Signaling Pathway.Recent patents on anti-cancer drug discovery · 2026Article
- The association between systemic immune-inflammation index and mortality of elderly chronic bronchitis patients complicated by acute myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- PCSK9 promotes atherosclerosis progression through the FOXO3a autophagy signaling pathway.Frontiers in cardiovascular medicine · 2026Article
- Targeting Macrophage-Mediated Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Strategies.Journal of inflammation research · 2026Review
- Screening of Anti-Atherosclerosis Targets of Ce-Bai-Si-Wei Decoction Based on Multidimensional Data and Study on Cellular Distribution.Journal of diabetes research · 2026Article
- Senescent macrophages in tumor: phenotypes, roles, and interventions.Cell death & disease · 2025Review
- Levo-corydalmine derived from Rhizoma Corydalis suppresses Ox-LDL-induced endothelial cell activation and improves vasodilatation by regulating the DDIT3-eNOS pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo investigate the process by which quercetin suppresses atherosclerosis by upregulating MST1-mediated autophagy in RAW264.7 macrophages.
methodsAn in vitro foam cell model was established by culturing RAW264.7 macrophages with oxidized low-density lipoprotein (ox-LDL). The cells were treated with quercetin alone or in combination with the autophagy inhibitor, 3-methyladenine, and autophagy agonist, rapamycin. Cell viability was detected with a CCK-8 kit. Lipid accumulation was detected by oil red O staining, senescence was detected by SA-β-gal (senescence-associated β-galactosidase) staining, reactive oxygen species were detected by ROS assay kit. Autophagosomes and mitochondria were detected by transmission electron microscope (TEM), and expression of MST1, LC3-II/I, Beclin1, Bcl-2, P21, and P16 were detected by immunofluorescence and Western blot.
resultsOx-LDL induced RAW264.7 macrophage-derived foam cell formation, reduced survival, aggravated cell lipid accumulation, and induced a senescence phenotype. This was accompanied by decreased formation of autophagosome; increased expression of P53, P21, and P16; and decreased expression of LC3-II/I and Beclin1. After intervention with quercetin, the cell survival rate was increased, and lipid accumulation and senescence phenotype were reduced. Furthermore, the expression of LC3-II/I and Beclin1 were increased, which was consistent with the ability of quercetin to promote autophagy. Ox-LDL also increased the expression of MST1, and this increase was blocked by quercetin, which provided a potential mechanism by which quercetin may protect foam cells against age-related detrimental effects.
conclusionQuercetin can inhibit the formation of foam cells induced by ox-LDL and delay senescence. The mechanism may be related to the regulation of MST1-mediated autophagy of RAW264.7 cells.
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.