ArticleImmunity2023
Cell-autonomous regulation of complement C3 by factor H limits macrophage efferocytosis and exacerbates atherosclerosis.
Article in Immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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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.
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Who cites it
49 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- Advances in Complement Research: from Pathophysiology to Precision Medicine.Physiology (Bethesda, Md.) · 2026Review
- Complement Activation by Post-Translationally Modified Proteins: Links to Chronic Inflammation and Autoimmunity.Immunological reviews · 2026Review
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Malondialdehyde epitopes exposed on dying cells are potent modulators of complement activity and efferocytosis.Journal of lipid research · 2026Article
- Transcriptomic, Specific Marker, and Pathway Analysis of Smooth Muscle Cell Foam Cells Relative to Macrophage Foam Cells in Human Atherosclerosis.bioRxiv : the preprint server for biology · 2026Article
- Urinary proteome and metabolome uncover tumor microenvironment and cellular metabolism changes of renal clear cell carcinoma.British journal of cancer · 2026Article
- 4-Octyl Itaconate Promotes Diabetic Wound Healing by Enhancing Pro-Resolving Macrophages via the Efferocytosis-MCT1-Lactate-GPR132 Pathway and Macrophage-Independent Synergistic Effects.Diabetes & metabolism journal · 2026Article
- Comprehensive Analysis of IgA Nephropathy Causal Factors in Plasma Proteins, Immune Cell Types, and Immune Cell Traits.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- Review
- Canadine protects against doxorubicin-induced cardiac and brain injury by inhibiting Oxidative stress.BMC pharmacology & toxicology · 2026Article
- Identification and clinical evaluation of diagnostic biomarkers for ischemic cardiomyopathy based on machine learning and transcriptomics.Frontiers in cardiovascular medicine · 2026Article
- Urinary CFHR2 as a Biomarker for Early Diagnosis and Disease Progression Prediction in Diabetic Kidney Disease.Current molecular medicine · 2026Article
- Integrative genetic and expression profiling prioritizesFrontiers in immunology · 2026Article
- A new perspective on AMD pathogenesis: a sequential Factor H-centered view of complement dysregulation.Frontiers in immunology · 2026Review
- Complement factor H in cancer biology: intracellular functions, tumor-host interactions, and systemic context.Frontiers in immunology · 2026Review
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- Role of monocytes in the pathogenesis of antiphospholipid syndrome and potential therapeutic targets (Review).Molecular medicine reports · 2025Review
- Emerging roles for complement in lung transplantation.The Journal of clinical investigation · 2025Review
- Inside job: Roles of intracellular C3.The Journal of allergy and clinical immunology · 2025Review
Corrections and comments
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Authors and funding
24 authors at 10 institutions in 5 countries.
Funding
Abstract
Complement factor H (CFH) negatively regulates consumption of complement component 3 (C3), thereby restricting complement activation. Genetic variants in CFH predispose to chronic inflammatory disease. Here, we examined the impact of CFH on atherosclerosis development. In a mouse model of atherosclerosis, CFH deficiency limited plaque necrosis in a C3-dependent manner. Deletion of CFH in monocyte-derived inflammatory macrophages propagated uncontrolled cell-autonomous C3 consumption without downstream C5 activation and heightened efferocytotic capacity. Among leukocytes, Cfh expression was restricted to monocytes and macrophages, increased during inflammation, and coincided with the accumulation of intracellular C3. Macrophage-derived CFH was sufficient to dampen resolution of inflammation, and hematopoietic deletion of CFH in atherosclerosis-prone mice promoted lesional efferocytosis and reduced plaque size. Furthermore, we identified monocyte-derived inflammatory macrophages expressing C3 and CFH in human atherosclerotic plaques. Our findings reveal a regulatory axis wherein CFH controls intracellular C3 levels of macrophages in a cell-autonomous manner, evidencing the importance of on-site complement regulation in the pathogenesis of inflammatory diseases.
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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.