ArticleJournal of immunology (Baltimore, Md. : 1950)2017
Complement Protein C1q Enhances Macrophage Foam Cell Survival and Efferocytosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 62 citations in OpenAlex.
- Complement Activation by Post-Translationally Modified Proteins: Links to Chronic Inflammation and Autoimmunity.Immunological reviews · 2026Review
- Exploratory LC-MS/MS-Based Proteomic and Lipidomic Profiling of Plasma Samples from Premature Coronary Artery Disease Patients: A Pilot Study in a South Asian Population.International journal of molecular sciences · 2026Article
- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- Targeting GPR34 in damage-associated macrophages enhances anti-tumor immunity and the efficacy of Surufatinib in pancreatic cancer.Signal transduction and targeted therapy · 2026Article
- Hypoxia-induced metabolic and apoptotic reprogramming enhances immunomodulation in Wharton's jelly mesenchymal stem cells.iScience · 2026Article
- Single cell spatial transcriptomics integration deciphers the morphological heterogeneity of atherosclerotic carotid arteries.Nature communications · 2025Article
- Macrophages Unmasked: Their Pivotal Role in Driving Atherosclerosis in Systemic Lupus Erythematosus.Clinical reviews in allergy & immunology · 2025Review
- Inflammatory Pathways in Coronary Artery Disease: Which Ones to Target for Secondary Prevention?Cells · 2025Review
- Article
- Phytochemical-mediated efferocytosis and autophagy in inflammation control.Cell death discovery · 2024Review
- Canonical and non-canonical roles of complement in atherosclerosis.Nature reviews. Cardiology · 2024Review
- Efferocytosis in atherosclerosis.Nature reviews. Cardiology · 2024Review
- Role of Complement in Liver Diseases.Seminars in liver disease · 2024Review
- Tissue-resident C1q + macrophages exert anti-aging potential through the Sirt1 pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The relationship between complement C1q and coronary plaque vulnerability based on optical coherence tomography analysis.Scientific reports · 2024Observational
- epHero - a tandem-fluorescent probe to track the fate of apoptotic cells during efferocytosis.Cell death discovery · 2024Article
- Macrophages Promote Atherosclerosis Development by Inhibiting CD8T Cell Apoptosis.Mediators of inflammation · 2024Article
- Consequence of alcohol intoxication-mediated efferocytosis impairment.Frontiers in immunology · 2024Review
- Complement C1q is a key player in tumor-associated macrophage-mediated CD8International journal of biological sciences · 2024Article
- The complement system in lipid-mediated pathologies.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
In the atherosclerotic lesion, macrophages ingest high levels of damaged modified low-density lipoproteins (LDLs), generating macrophage foam cells. Foam cells undergo apoptosis and, if not efficiently cleared by efferocytosis, can undergo secondary necrosis, leading to plaque instability and rupture. As a component of the innate immune complement cascade, C1q recognizes and opsonizes modified forms of LDL, such as oxidized or acetylated LDL, and promotes ingestion by macrophages in vitro. C1q was shown to be protective in an atherosclerosis model in vivo. Therefore, this study aimed to investigate whether ingestion of modified LDL in the presence of C1q alters macrophage foam cell survival or function. In an unbiased transcriptome analysis, C1q was shown to modulate expression of clusters of genes involved in cell death and apoptosis pathways in human monocyte-derived macrophages ingesting modified LDL; this was validated by quantitative PCR in human and murine macrophages. C1q downregulated levels and activity of active caspase-3 and PARP-1 in human and mouse macrophages during ingestion of modified LDL. This led to a measurable increase in survival and decrease in cell death, as measured by alamarBlue and propidium iodide assays, respectively. C1q opsonization also increased phagocytosis and efferocytosis in macrophage foam cells. These data suggest that C1q promotes macrophage survival during ingestion of excess cholesterol, as well as improves foam cell efferocytic function. This may be important in slowing disease progression and provides insight into the protective role of C1q in early atherosclerosis.
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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.