ReviewImmunity2017
Monocyte-Macrophages and T Cells in Atherosclerosis.
Review in Immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 354 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
354 citing papers in PubMed, 1 synthesis or guideline pooled it, 635 citations in OpenAlex.
- Natural killer cells in preeclampsia: an overview of current research.Frontiers in immunology · 2026Pooled it
- Multi-omics integration and machine learning identify an ACKR1Clinical and translational medicine · 2026Article
- Lactylation at the metabolic-epigenetic interface in cardiovascular diseases: context-dependent mechanisms and translational roadmap.Journal of advanced research · 2026Review
- Dendritic Cells in the Immunoregulation of Myocardial Infarction: Mechanisms and Therapeutic Strategies.Cardiovascular drugs and therapy · 2026Review
- Nuclear RSK1 mediates interferon-γ-induced proinflammatory activation in human primary macrophages and humanized mice.Science advances · 2026Article
- Targeting Inflammation in Atherosclerotic Cardiovascular Disease: Mechanisms and Emerging Therapies.Immunological reviews · 2026Review
- Incretin-Based Therapies, Obesity-Associated Inflammation, and Atherosclerotic Cardiovascular Risk.Cells · 2026Review
- Age-associated decline of Lamtor5 drives immunosenescence and systemic aging via cGAS-mediated paracrine inflammation.Cell death and differentiation · 2026Article
- Review
- PCSK9 in critical illness - It's not all about lipids.Annals of clinical biochemistry · 2026Review
- Environmental Exposure to Micro- and Nanoplastics: Linking Cardiovascular Disease and Cancer Through Shared Biological Pathways-A Critical Review.Antioxidants (Basel, Switzerland) · 2026Review
- Cell-derived vesicle-modified biomaterials for tissue repair and regeneration.Materials today. Bio · 2026Review
- Macrophage metabolism reprogramming in sepsis: Pathogenesis and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- CD8Nature reviews. Cardiology · 2026Review
- Nanomedicine-based theranostics in atherosclerotic cardiovascular diseases.Journal of biomedical science · 2026Review
- Mechanisms, precision therapies, and technological frontiers in coronary atherosclerosis: a comprehensive review.Acta pharmacologica Sinica · 2026Review
- Tussilagone mitigates sepsis-induced acute lung injury in mice by suppressing RIPK1 expression.Hereditas · 2026Article
- Artery tertiary lymphoid organs, neuro-immune interaction and their mediators in atherosclerosis.Basic research in cardiology · 2026Review
- Telomerase Knockout in Myeloid Cells Predisposes Mice to Foam Cell Formation, Dyslipidemia, Lung Fibrosis, and Cardiac Dysfunction.Aging cell · 2026Article
- IL-12-secreting CAR-T cells reprogram the tumor microenvironment and improve efficacy against heterogeneous models of glioblastoma.Journal for immunotherapy of cancer · 2026Article
294 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Atherosclerosis is an arterial disease process characterized by the focal subendothelial accumulation of apolipoprotein-B-containing lipoproteins, immune and vascular wall cells, and extracellular matrix. The lipoproteins acquire features of damage-associated molecular patterns and trigger first an innate immune response, dominated by monocyte-macrophages, and then an adaptive immune response. These inflammatory responses often become chronic and non-resolving and can lead to arterial damage and thrombosis-induced organ infarction. The innate immune response is regulated at various stages, from hematopoiesis to monocyte changes and macrophage activation. The adaptive immune response is regulated primarily by mechanisms that affect the balance between regulatory and effector T cells. Mechanisms related to cellular cholesterol, phenotypic plasticity, metabolism, and aging play key roles in affecting these responses. Herein, we review select topics that shed light on these processes and suggest new treatment strategies.
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.