ReviewFrontiers in immunology2023
Macrophage death in atherosclerosis: potential role in calcification.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 39 citations in OpenAlex.
- Systemic inflammation increases mast cell numbers in coronary arteries in patients who died from myocardial infarction.Journal of molecular and cellular cardiology plus · 2026Article
- Statin Use and Arterial Calcification in the General Population: A Longitudinal Analysis and a Negative Control Population.Clinical drug investigation · 2026Article
- Diabetic plaque calcification: mechanisms, imaging phenotypes, and clinical implications.npj metabolic health and disease · 2026Review
- Coronary Calcified Nodules: From Pathological Definitions to Intravascular Imaging- and Morphology-Guided PCI.International journal of molecular sciences · 2026Review
- Microcalcification: Effects on Atherosclerotic Vulnerable Plaques, Detection, and Therapeutic Perspectives.Current atherosclerosis reports · 2026Review
- Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026Review
- Single-cell spatial transcriptomics reveals clonal smooth muscle cell heterogeneity and programs associated with atherosclerotic plaque calcification.Clinical and experimental medicine · 2026Article
- Targeting B7-H3 attenuates uremic vascular calcification by suppressing phenotypic switching of VSMCs and regulating VSMCs-macrophage crosstalk.Clinical and experimental nephrology · 2026Article
- From uric acid to tophi: multistage molecular and cellular mechanisms of tophi formation.Frontiers in immunology · 2026Review
- Targeting vascular inflammation and endothelial dysfunction with nanobodies: emerging therapeutic strategies for cardiovascular disease.Frontiers in immunology · 2026Review
- Ferroptosis in arterial atherosclerosis: mechanistic hypotheses, cell type specific vulnerabilities, translational biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity.Frontiers in immunology · 2026Review
- Calcifying nanoparticles induce apoptosis and calcification in bone marrow mesenchymal stem cellsWorld journal of stem cells · 2025Article
- Gold Nanoparticles in Atherosclerosis: A Dual Approach to Diagnosis and Therapy.Molecular imaging and biology · 2025Review
- Comprehensive Review of Mechanisms and Translational Perspectives on Programmed Cell Death in Vascular Calcification.Biomolecules · 2025Review
- Anti-inflammatory interventions in coronary artery disease: antipodal responses requiring targeted therapeutic strategies.Basic research in cardiology · 2025Review
- Calcium Signaling Dynamics in Vascular Cells and Their Dysregulation in Vascular Disease.Biomolecules · 2025Review
- Inflammasome Activation and Neutrophil Extracellular Traps in Atherosclerosis.Journal of atherosclerosis and thrombosis · 2025Review
- WTAP Promotes Atherosclerosis by Inducing Macrophage Pyroptosis and M1 Polarization through Upregulating NLRP3.Applied biochemistry and biotechnology · 2025Article
- The novel GSDMD inhibitor GI-Y2 exerts antipyroptotic effects to reduce atherosclerosis.Clinical and translational medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell death is an important aspect of atherosclerotic plaque development. Insufficient efferocytosis of death cells by phagocytic macrophages leads to the buildup of a necrotic core that impacts stability of the plaque. Furthermore, in the presence of calcium and phosphate, apoptotic bodies resulting from death cells can act as nucleation sites for the formation of calcium phosphate crystals, mostly in the form of hydroxyapatite, which leads to calcification of the atherosclerotic plaque, further impacting plaque stability. Excessive uptake of cholesterol-loaded oxidized LDL particles by macrophages present in atherosclerotic plaques leads to foam cell formation, which not only reduces their efferocytosis capacity, but also can induce apoptosis in these cells. The resulting apoptotic bodies can contribute to calcification of the atherosclerotic plaque. Moreover, other forms of macrophage cell death, such as pyroptosis, necroptosis, parthanatos, and ferroptosis can also contribute by similar mechanisms to plaque calcification. This review focuses on macrophage death in atherosclerosis, and its potential role in calcification. Reducing macrophage cell death and/or increasing their efferocytosis capacity could be a novel therapeutic strategy to reduce the formation of a necrotic core and calcification and thereby improving atherosclerotic plaque stability.
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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.