ArticleArteriosclerosis, thrombosis, and vascular biology2021
ODC (Ornithine Decarboxylase)-Dependent Putrescine Synthesis Maintains MerTK (MER Tyrosine-Protein Kinase) Expression to Drive Resolution.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 49 citations in OpenAlex.
- Efferocytosis activates a DNMT3A-mediated oxidized DNA repair pathway to enable tissue resolution.The Journal of clinical investigation · 2026Article
- Metabolic Pathways Linking Atherosclerotic Cardiovascular Disease With Metabolic Dysfunction-Associated Steatotic Liver Disease.Current atherosclerosis reports · 2026Review
- Hypothermic machine perfusion protects DCD graft liver from ischemia‑reperfusion injury by enhancing macrophage efferocytosis via KLF2‑NLRP3 signaling.International journal of molecular medicine · 2026Article
- Myeloid HDAC3 deletion protects against traumatic optic injury.Cell death discovery · 2026Article
- Efferocytosis-Driven Polyamine Metabolism in Macrophages Enhances Cancer Stem Cell Enrichment after Chemotherapy in Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Efferocytosis: the art of cellular clearance and novel perspectives in disease therapy.Molecular cancer · 2025Review
- Activated protein C ameliorates diabetes-induced atherosclerosis by sustaining macrophage efferocytosis.Cardiovascular diabetology · 2025Article
- Macrophage WDFY3 mitigates autoimmunity by enhancing efferocytosis and suppressing T cell activation in mice.Nature communications · 2025Article
- Anti-Atherogenic Mechanisms and Therapies.Current atherosclerosis reports · 2025Review
- The Atherosclerotic Plaque Microenvironment as a Therapeutic Target.Current atherosclerosis reports · 2025Review
- Matrix-Rigidity Cooperates With Biochemical Cues in M2 Macrophage Activation Through Increased Nuclear Deformation and Chromatin Accessibility.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Lipin-1 restrains macrophage lipid synthesis to promote inflammation resolution.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Macrophages in osteoporotic fractures: from immunometabolic mechanisms to precision therapeutic approaches.Frontiers in endocrinology · 2025Review
- Structure simulation-based comparison of active site variations in fungal ornithine decarboxylases.Communicative & integrative biology · 2025Article
- Efferocytosis in atherosclerosis.Nature reviews. Cardiology · 2024Review
- Article
- Efferocytosis drives a tryptophan metabolism pathway in macrophages to promote tissue resolution.Nature metabolism · 2024Article
- Macrophage WDFY3, a protector against autoimmunity.bioRxiv : the preprint server for biology · 2024Article
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury.Journal of neuroinflammation · 2024Article
- Mechanism of efferocytosis in atherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2024Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveODC (ornithine decarboxylase)-dependent putrescine synthesis promotes the successive clearance of apoptotic cells (ACs) by macrophages, contributing to inflammation resolution. However, it remains unknown whether ODC is required for other arms of the resolution program. Approach and Results: RNA sequencing of ODC-deficient macrophages exposed to ACs showed increases in mRNAs associated with heightened inflammation and decreases in mRNAs related to resolution and repair compared with WT (wild type) macrophages. In zymosan peritonitis, myeloid ODC deletion led to delayed clearance of neutrophils and a decrease in the proresolving cytokine, IL (interleukin)-10. Nanoparticle-mediated silencing of macrophage ODC in a model of atherosclerosis regression lowered IL-10 expression, decreased efferocytosis, enhanced necrotic core area, and reduced fibrous cap thickness. Mechanistically, ODC deletion lowered basal expression of MerTK (MER tyrosine-protein kinase)-an AC receptor-via a histone methylation-dependent transcriptional mechanism. Owing to lower basal MerTK, subsequent exposure to ACs resulted in lower MerTK-Erk (extracellular signal-regulated kinase) 1/2-dependent IL-10 production. Putrescine treatment of ODC-deficient macrophages restored the expression of both MerTK and AC-induced IL-10.
conclusionsThese findings demonstrate that ODC-dependent putrescine synthesis in macrophages maintains a basal level of MerTK expression needed to optimally resolve inflammation upon subsequent AC exposure. Graphic Abstract: A graphic abstract is available for this article.
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