ReviewJournal of atherosclerosis and thrombosis2020
An Update on the Role of PCSK9 in Atherosclerosis.
Review in Journal of atherosclerosis and thrombosis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis 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
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Pooled it
- The efficacy of preoperative evolocumab-rosuvastatin combination therapy in patients with ST-elevation myocardial infarction.PloS one · 2026Trial
- Trial
- Proprotein Convertase Subtilisin/Kexin Type 9 and Systemic Inflammatory Biomarker Pentraxin 3 for Risk Stratification Among STEMI Patients Undergoing Primary PCI.Journal of inflammation research · 2021Trial
- Hexosamine Biosynthetic Pathway and Fatty Acid β-Oxidative Imbalance: A Key Mechanism by Which Abnormal Macrophage Lipophagy Promotes Atherosclerosis in Diabetes.Cardiovascular drugs and therapy · 2026Review
- Mouse Models of Atherosclerosis: What They Teach Us, What They Miss, and When to Use Them.Bioengineering (Basel, Switzerland) · 2026Review
- Regulation of PCSK9 During Oxidized LDL-Induced Foam Cell Formation in RAW264.7 Cells.Biology · 2026Article
- uPAR-Guided Dendrimer Gel Nanoparticles Reprogram Inflammation to Stabilize Atherosclerotic Plaques.ACS applied materials & interfaces · 2026Article
- Review
- HJournal of nanobiotechnology · 2026Article
- PCSK9 in vascular smooth muscle cells: biology, pathology, and inhibition to fight atherosclerosis.Atherosclerosis plus · 2026Review
- Therapeutic Potential of PCSK9 Inhibitors in Regulating Neuroinflammation in Acute Ischemic Stroke.CNS drugs · 2026Review
- Mechanistic insights into the lipotropic and atheroprotective effects of rosuvastatin-loaded glycerosomes in dyslipidemic rats.Scientific reports · 2026Article
- Review
- PCSK9 promotes atherosclerosis progression through the FOXO3a autophagy signaling pathway.Frontiers in cardiovascular medicine · 2026Article
- Proactive, short-term PCSK9 inhibition after PCI in patients with coronary artery disease at high residual risk: rationale and design of the randomized HANYANG-PICK trial.Frontiers in cardiovascular medicine · 2026Article
- PCSK9 and coronary atherosclerosis progression beyond LDL-cholesterol in coronary artery disease patients.European journal of clinical investigation · 2025Article
- Association Between HNP1-3 and Atherosclerotic Plaque Burden in Subclinical Atherosclerosis and the Mediating Effect of PCSK9.Clinical and translational science · 2025Article
- Endothelial Cell-Derived PCSK9 in Atherosclerosis: Pathophysiological Roles and Therapeutic Perspectives.Reviews in cardiovascular medicine · 2025Review
- Intersecting Pathways of Inflammation, Oxidative Stress, and Atherogenesis in the Evaluation of CKD: Emerging Biomarkers PCSK9, EPHX2, AOPPs, and TBARSs.Life (Basel, Switzerland) · 2025Review
8 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
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is initiated by functional changes in the endothelium accompanied by accumulation, oxidation, and glycation of LDL-cholesterol in the inner layer of the arterial wall and continues with the expression of adhesion molecules and release of chemoattractants. PCSK9 is a proprotein convertase that increases circulating LDL levels by directing hepatic LDL receptors into lysosomes for degradation. The effects of PCSK9 on hepatic LDL receptors and contribution to atherosclerosis via the induction of hyperlipidemia are well defined. Monoclonal PCSK9 antibodies that block the effects of PCSK9 on LDL receptors demonstrated beneficial results in cardiovascular outcome trials. In recent years, extrahepatic functions of PCSK9, particularly its direct effects on atherosclerotic plaques have received increasing attention. Experimental trials have revealed that PCSK9 plays a significant role in every step of atherosclerotic plaque formation. It contributes to foam cell formation by increasing the uptake of LDL by macrophages via scavenger receptors and inhibiting cholesterol efflux from macrophages. It induces the expression of inflammatory cytokines, adhesion molecules, and chemoattractants, thereby increasing monocyte recruitment, inflammatory cell adhesion, and inflammation at the atherosclerotic vascular wall. Moreover, low shear stress is associated with increased PCSK9 expression. PCSK9 may induce endothelial cell apoptosis and autophagy and stimulate the differentiation of smooth muscle cells from the contractile phenotype to synthetic phenotype. Increasing evidence indicates that PCSK9 is a molecular target in the development of novel approaches toward the prevention and treatment of atherosclerosis. This review focuses on the molecular roles of PCSK9 in atherosclerotic plaque formation.
Indexed as
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What Socratic 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 Socratic graph.