ReviewArteriosclerosis, thrombosis, and vascular biology2017
2016 Russell Ross Memorial Lecture in Vascular Biology: Molecular-Cellular Mechanisms in the Progression of Atherosclerosis.
Review in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Interleukin-receptor antagonist and tumour necrosis factor inhibitors for the primary and secondary prevention of atherosclerotic cardiovascular diseases.The Cochrane database of systematic reviews · 2024Pooled it
- Unmet Cardiovascular Risk Beyond LDL-C: A Perspective on Managing Residual Cardiovascular Risk.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Endothelial ferroptosis: a novel mechanism and therapeutic target in diabetic microvascular complications.Molecular medicine (Cambridge, Mass.) · 2026Review
- Nutriepigenetics and nutriepigenomics: Exploring the interactions between nutrition, epigenetics, and epigenomics in the pathogenesis of noncommunicable diseases.Genetics and molecular biology · 2026Article
- Intimal Macrovascular Pericytes: Their Role in Vascular Biology and Atherogenesis.Current medicinal chemistry · 2025Review
- Phytochemical-mediated efferocytosis and autophagy in inflammation control.Cell death discovery · 2024Review
- Review
- Exploratory Study of Differentially Expressed Genes of Peripheral Blood Monocytes in Patients with Carotid Atherosclerosis.Combinatorial chemistry & high throughput screening · 2024Article
- NSUN6 and HTR7 disturbed the stability of carotid atherosclerotic plaques by regulating the immune responses of macrophages.Open medicine (Warsaw, Poland) · 2024Article
- Rap1 in the Context of PCSK9, Atherosclerosis, and Diabetes.Current atherosclerosis reports · 2023Review
- PPARγ in Atherosclerotic Endothelial Dysfunction: Regulatory Compounds and PTMs.International journal of molecular sciences · 2023Review
- Can Electronegative LDL Act as a Multienzymatic Complex?International journal of molecular sciences · 2023Review
- CD14International journal of molecular sciences · 2023Article
- Human IL-32θA94V mutant attenuates monocyte-endothelial adhesion by suppressing the expression of ICAM-1 and VCAM-1 via binding to cell surface receptor integrin αVβ3 and αVβ6 in TNF-α-stimulated HUVECs.Frontiers in immunology · 2023Article
- Apolipoprotein E in Cardiometabolic and Neurological Health and Diseases.International journal of molecular sciences · 2022Review
- The Role of Peroxisome Proliferator-Activated Receptor Gamma and Atherosclerosis: Post-translational Modification and Selective Modulators.Frontiers in physiology · 2022Review
- Nutritional Epigenetics: How Metabolism Epigenetically Controls Cellular Physiology, Gene Expression and Disease.Sub-cellular biochemistry · 2022Article
- Defective efferocytosis of vascular cells in heart disease.Frontiers in cardiovascular medicine · 2022Review
- The Endothelium as a Hub for Cellular Communication in Atherogenesis: Is There Directionality to the Message?Frontiers in cardiovascular medicine · 2022Review
- Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Atherosclerosis is initiated by the subendothelial accumulation of apoB-lipoproteins, which initiates a sterile inflammatory response dominated by monocyte-macrophages but including all classes of innate and adaptive immune cells. These inflammatory cells, together with proliferating smooth muscle cells and extracellular matrix, promote the formation of subendothelial lesions or plaques. In the vast majority of cases, these lesions do not cause serious clinical symptoms, which is due in part to a resolution-repair response that limits tissue damage. However, a deadly minority of lesions progress to the point where they can trigger acute lumenal thrombosis, which may then cause unstable angina, myocardial infarction, sudden cardiac death, or stroke. Many of these clinically dangerous lesions have hallmarks of defective inflammation resolution, including defective clearance of dead cells (efferocytosis), necrosis, a defective scar response, and decreased levels of lipid mediators of the resolution response. Efferocytosis is both an effector arm of the resolution response and an inducer of resolution mediators, and thus its defect in advanced atherosclerosis amplifies plaque progression. Preclinical causation/treatment studies have demonstrated that replacement therapy with exogenously administered resolving mediators can improve lesional efferocytosis and prevent plaque progression. Work in this area has the potential to potentiate the cardiovascular benefits of apoB-lipoprotein-lowering therapy.
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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.