ArticleJCI insight2018
Glucose metabolism controls disease-specific signatures of macrophage effector functions.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 87 citations in OpenAlex.
- cAMP-response element binding protein (CREB)-mediated glycolysis enhancement promotes apoptosis of RAW264.7 macrophages infected with BCG under high glucose conditions.BMC microbiology · 2026Article
- Unraveling Immune Checkpoint Inhibitor-Associated Cardiovascular Toxicities: Pathway Insights, Mechanisms, and Emerging Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- Persistent glycolysis defines pathological foreign body-associated inflammation to polymeric implants.Science advances · 2025Article
- Review
- Monocytes/Macrophages in Giant Cell Arteritis-Polymyalgia Rheumatica Spectrum Disease.Aging and disease · 2025Review
- The role of myocardial fibrosis in the diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2025Review
- Metabolism Serves as a Bridge Between Cardiomyocytes and Immune Cells in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2025Review
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Roles of circadian clocks in macrophage metabolism: implications in inflammation and metabolism of lipids, glucose, and amino acids.American journal of physiology. Endocrinology and metabolism · 2025Review
- Mitochondrial Dysfunction and Atherosclerosis: The Problem and the Search for Its Solution.Biomedicines · 2025Review
- Metabolic checkpoints in rheumatoid arthritis.Seminars in arthritis and rheumatism · 2025Review
- Metabolic Homeostasis of Immune Cells Modulates Cardiovascular Diseases.Research (Washington, D.C.) · 2025Review
- Immune Checkpoints Are New Therapeutic Targets in Regulating Cardio-, and Cerebro-Vascular Diseases and CD4International journal of drug discovery and pharmacology · 2024Article
- Crosstalk between macrophages and immunometabolism and their potential roles in tissue repair and regeneration.Heliyon · 2024Review
- Loss of synovial tissue macrophage homeostasis precedes rheumatoid arthritis clinical onset.Science advances · 2024Article
- Review
- Atorvastatin ameliorated myocardial fibrosis in db/db mice by inhibiting oxidative stress and modulating macrophage polarization.World journal of diabetes · 2023Article
- Oncolytic viruses improve cancer immunotherapy by reprogramming solid tumor microenvironment.Medical oncology (Northwood, London, England) · 2023Review
- The role of cardiac resident macrophage in cardiac aging.Aging cell · 2023Review
- SEMA4D/VEGF surface enhances endothelialization by diminished-glycolysis-mediated M2-like macrophage polarization.Materials today. Bio · 2023Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundIn inflammatory blood vessel diseases, macrophages represent a key component of the vascular infiltrates and are responsible for tissue injury and wall remodeling.
methodsTo examine whether inflammatory macrophages in the vessel wall display a single distinctive effector program, we compared functional profiles in patients with either coronary artery disease (CAD) or giant cell arteritis (GCA).
resultsUnexpectedly, monocyte-derived macrophages from the 2 patient cohorts displayed disease-specific signatures and differed fundamentally in metabolic fitness. Macrophages from CAD patients were high producers for T cell chemoattractants (CXCL9, CXCL10), the cytokines IL-1β and IL-6, and the immunoinhibitory ligand PD-L1. In contrast, macrophages from GCA patients upregulated production of T cell chemoattractants (CXCL9, CXCL10) but not IL-1β and IL-6, and were distinctly low for PD-L1 expression. Notably, disease-specific effector profiles were already identifiable in circulating monocytes. The chemokinehicytokinehiPD-L1hi signature in CAD macrophages was sustained by excess uptake and breakdown of glucose, placing metabolic control upstream of inflammatory function.
conclusionsWe conclude that monocytes and macrophages contribute to vascular inflammation in a disease-specific and discernible pattern, have choices to commit to different functional trajectories, are dependent on glucose availability in their immediate microenvironment, and possess memory in their lineage commitment.
fundingSupported by the NIH (R01 AR042527, R01 HL117913, R01 AI108906, P01 HL129941, R01 AI108891, R01 AG045779 U19 AI057266, R01 AI129191), I01 BX001669, and the Cahill Discovery Fund.
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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.