SynthesisFrontiers in immunology2022
Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation.
Synthesis in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 82 citations in OpenAlex.
- Sinomenine protects against oxidized low-density lipoprotein-induced human umbilical vein endothelial cell injury through regulating the myocyte enhancer factor 2 A/C-X-C motif chemokine ligand 14 pathway.Journal of bioenergetics and biomembranes · 2026Article
- Macrophage Plasticity: Phenotypic and Functional Profiles Across Pathological Microenvironments.International journal of molecular sciences · 2026Review
- The Relationship and Mechanism of CD27 with Coronary Atherosclerotic Heart Disease.Cardiovascular drugs and therapy · 2026Review
- Overexpression of miR-7641 activates ox-LDL-induced autophagy in macrophages by regulating USP7.Molecular biology reports · 2026Article
- Ring finger protein 10 is atherosclerosis protective and modulates macrophage polarization.Experimental animals · 2026Article
- The Role of Glutathione Peroxidase 4 in Atherosclerosis: Role and Therapeutic Potential.Reviews in cardiovascular medicine · 2026Review
- Reactive Oxygen and Nitrogen Species on Monocyte and Macrophage Biology.Antioxidants (Basel, Switzerland) · 2026Review
- The Mental Health-Acute Coronary Syndrome Continuum: Bidirectional Pathophysiological Links and Clinical Implications.Medical sciences (Basel, Switzerland) · 2026Review
- Exposure to a PFAS mixture alters cholesterol lipoprotein subfractions and induces a foam cell-like aortic macrophage expression profile in hyperlipidemic LDLrToxicology and applied pharmacology · 2026Article
- Mechanistic insights and challenges in mitochondrial regulation of macrophage polarization and inflammatory responses.Frontiers in physiology · 2026Review
- Novel insights of ferroptosis in atherosclerosis progression.Frontiers in cell and developmental biology · 2026Review
- SEMA4A signaling in macrophage subpopulations and its implication in osteoarthritis.Frontiers in immunology · 2026Article
- Ferroptosis in arterial atherosclerosis: mechanistic hypotheses, cell type specific vulnerabilities, translational biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Microbiota-innate immune crosstalk drives atherosclerosis: mechanisms, disease progression, and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- The dual role of metabolic reprogramming in macrophage polarization in rheumatoid arthritis and coronary heart disease and the intervention strategy of traditional Chinese medicine.Frontiers in cardiovascular medicine · 2026Review
- Caspase Recruitment Domain Family Member 8: A Favorable Target in the Pathogenesis of Atherosclerosis.Reviews in cardiovascular medicine · 2026Review
- Reappraising heme oxygenase-1 as a ferroptosis modulator in atherosclerosis: a mechanism-focused review.Frontiers in immunology · 2026Review
- Spatio-temporal dynamics of autophagy-associated genes in macrophage-driven atherosclerosis: an integrated omics and experimental study.Frontiers in endocrinology · 2026Article
- Protein lactylation influences atherosclerotic plaque stability by regulating macrophage functions.Frontiers in immunology · 2026Review
- RORα: a critical nexus in the crosstalk between cholesterol metabolism and macrophage polarization.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases, the notorious killer, are mainly caused by atherosclerosis (AS) characterized by lipids, cholesterol, and iron overload in plaques. Macrophages are effector cells and accumulate to the damaged and inflamed sites of arteries to internalize native and chemically modified lipoproteins to transform them into cholesterol-loaded foam cells. Foam cell formation is determined by the capacity of phagocytosis, migration, scavenging, and the features of phenotypes. Macrophages are diverse, and the subsets and functions are controlled by their surrounding microenvironment. Generally, macrophages are divided into classically activated (M1) and alternatively activated (M2). Recently, intraplaque macrophage phenotypes are recognized by the stimulation of CXCL4 (M4), oxidized phospholipids (Mox), hemoglobin/haptoglobin complexes [HA-mac/M(Hb)], and heme (Mhem). The pro-atherogenic or anti-atherosclerotic phenotypes of macrophages decide the progression of AS. Besides, apoptosis, necrosis, ferroptosis, autophagy and pyrotopsis determine plaque formation and cardiovascular vulnerability, which may be associated with macrophage polarization phenotypes. In this review, we first summarize the three most popular hypotheses for AS and find the common key factors for further discussion. Secondly, we discuss the factors affecting macrophage polarization and five types of macrophage death in AS progression, especially ferroptosis. A comprehensive understanding of the cellular and molecular mechanisms of plaque formation is conducive to disentangling the candidate targets of macrophage-targeting therapies for clinical intervention at various stages of AS.
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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.