ReviewScientifica2015
Macrophage Heterogeneity and Plasticity: Impact of Macrophage Biomarkers on Atherosclerosis.
Review in Scientifica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- Interplay Between KLF4, STAT, IRF, and NF-κB in VSMC and Macrophage Plasticity During Vascular Inflammation and Atherosclerosis.International journal of molecular sciences · 2025Review
- Spatial metabolic and phenotypic characterization of the germ-free mouse model.Annals of the New York Academy of Sciences · 2025Article
- Immunoregulatory iPSC-derived non-lymphoid progeny in autoimmunity and GVHD alloimmunity.Stem cells (Dayton, Ohio) · 2025Review
- Neuroprotective Effects of AER-271 in a tMCAO Mouse Model: Modulation of Autophagy, Apoptosis, and Inflammation.Inflammation · 2025Article
- Unveiling TIMPs: A Systematic Review of Their Role as Biomarkers in Atherosclerosis and Coronary Artery Disease.Diseases (Basel, Switzerland) · 2024Review
- Regulatory T cells and macrophages in atherosclerosis: from mechanisms to clinical significance.Frontiers in immunology · 2024Review
- Immunohistochemical Characterization of M1, M2, and M4 Macrophages in Leprosy Skin Lesions.Pathogens (Basel, Switzerland) · 2023Article
- Regulatory Mechanism of M1/M2 Macrophage Polarization in the Development of Autoimmune Diseases.Mediators of inflammation · 2023Review
- Activation of circulating monocytes by low-density lipoprotein-a risk factor for osteoarthritis?Rheumatology (Oxford, England) · 2022Article
- Specialized Proresolving Lipid Mediators: A Potential Therapeutic Target for Atherosclerosis.International journal of molecular sciences · 2022Review
- Lipid-Laden Macrophages and Inflammation in AtherosclerosiFrontiers in cardiovascular medicine · 2022Review
- The effects of a biodegradable Mg-based alloy on the function of VSMCs via immunoregulation of macrophages through Mg-induced responses.Annals of translational medicine · 2021Article
- The correlation between tumor-associated macrophage infiltration and progression in cervical carcinoma.Bioscience reports · 2021Article
- Interleukins and Interleukin Receptors Evolutionary History and Origin in Relation to CD4+ T Cell Evolution.Genes · 2021Article
- Galectin 3 and non-classical monocytes of blood as myocardial remodeling factors at ischemic cardiomyopathy.International journal of cardiology. Heart & vasculature · 2021Article
- Review
- Macrophage-Based Therapies for Atherosclerosis Management.Journal of immunology research · 2020Review
- Attenuation of Diabetic Nephropathy in Diabetic Mice by Fasudil through Regulation of Macrophage Polarization.Journal of diabetes research · 2020Article
- Adoptive transfer of polarized M2c macrophages ameliorates acute rejection in rat liver transplantation.American journal of translational research · 2020Article
- M2b macrophage polarization and its roles in diseases.Journal of leukocyte biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease (CVD) is a global epidemic, currently representing the worldwide leading cause of morbidity and mortality. Atherosclerosis is the fundamental pathophysiologic component of CVD, where the immune system plays an essential role. Monocytes and macrophages are key mediators in this aspect: due to their heterogeneity and plasticity, these cells may act as either pro- or anti-inflammatory mediators. Indeed, monocytes may develop heterogeneous functional phenotypes depending on the predominating pro- or anti-inflammatory microenvironment within the lesion, resulting in classic, intermediate, and non-classic monocytes, each with strikingly differing features. Similarly, macrophages may also adopt heterogeneous profiles being mainly M1 and M2, the former showing a proinflammatory profile while the latter demonstrates anti-inflammatory traits; they are further subdivided in several subtypes with more specialized functions. Furthermore, macrophages may display plasticity by dynamically shifting between phenotypes in response to specific signals. Each of these distinct cell profiles is associated with diverse biomarkers which may be exploited for therapeutic intervention, including IL-10, IL-13, PPAR-γ, LXR, NLRP3 inflammasomes, and microRNAs. Direct modulation of the molecular pathways concerning these potential macrophage-related targets represents a promising field for new therapeutic alternatives in atherosclerosis and CVD.
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.