ArticleEMBO molecular medicine2023
Enhancement of efferocytosis through biased FPR2 signaling attenuates intestinal inflammation.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- FPR1-Driven Neutrophil-Endothelial Cell Axis Promotes Angiogenesis in PAOD.Circulation research · 2026Article
- Toward a Therapy for Autism Spectrum Disorder: The Formyl Peptide Receptor 2 Agonist MR-39 Supports Synaptic Health in the BTBR Mouse and Features a Favorable Safety Profile.ACS pharmacology & translational science · 2026Article
- Macrophage efferocytosis promotes inflammation resolution and accelerates wound healing.Communications biology · 2026Review
- LC3-associated phagocytosis is impaired in monocyte-derived macrophages from systemic sclerosis patients.Autophagy reports · 2026Article
- Impaired Macrophage Efferocytosis: Shared Mechanisms and Therapeutic Implications in Immune-Mediated Inflammatory Diseases.Journal of inflammation research · 2026Review
- Advancements in nanomedicine for the therapeutic regulation of efferocytosis: opportunities and challenges.Theranostics · 2026Review
- Targeting efferocytosis for tissue regeneration: From microenvironment reprogramming to clinical translation.Theranostics · 2026Review
- Synergistic enhancement of efferocytosis and cholesterol efflux via macrophage biomimetic nanoparticle to attenuate atherosclerosis progression.Bioactive materials · 2026Article
- Efferocytosis in tissue engineering: A comprehensive review of emerging therapeutic strategies for enhanced tissue repair and regeneration.Bioactive materials · 2025Review
- Identification of Key Efferocytosis-Related Genes and Mechanisms in Diabetic Retinopathy.Molecular biotechnology · 2025Article
- Oral FPR2/ALX modulators tune myeloid cell activity to ameliorate mucosal inflammation in inflammatory bowel disease.Acta pharmacologica Sinica · 2025Article
- Formyl peptide receptor 2: a potential therapeutic target for inflammation-related diseases.Pharmacological reports : PR · 2025Review
- LGR6 modulates intervertebral disc degeneration through regulation of macrophage efferocytosis.Journal of translational medicine · 2025Article
- Role of FPR2 antagonism in alleviating social isolation-induced depression and protecting blood-brain barrier integrity.Journal of neuroinflammation · 2025Article
- Emerging paradigms for target discovery of traditional medicines: A genome-wide pan-GPCR perspective.Innovation (Cambridge (Mass.)) · 2025Review
- Multi-omics reveals efferocytosis-related hub genes as biomarkers for ustekinumab response in colitis.Frontiers in immunology · 2025Article
- Annexin A1 and A2 in inflammatory bowel disease pathogenesis: exploring new avenues for diagnosis and treatment.Frontiers in immunology · 2025Review
- EDIL3/Del-1 prevents aortic dissection through enhancing internalization and degradation of apoptotic vascular smooth muscle cells.Autophagy · 2024Article
- Synthetic Biomimetic Liposomes Harness Efferocytosis Machinery for Highly Efficient Macrophages-Targeted Drug Delivery to Alleviate Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Macrophage Perspectives in Liver Diseases: Programmed Death, Related Biomarkers, and Targeted Therapy.Biomolecules · 2024Review
Corrections and comments
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Authors and funding
19 authors at 9 institutions in 3 countries.
Funding
Abstract
Efficient clearance of dying cells (efferocytosis) is an evolutionarily conserved process for tissue homeostasis. Genetic enhancement of efferocytosis exhibits therapeutic potential for inflammation resolution and tissue repair. However, pharmacological approaches to enhance efferocytosis remain sparse due to a lack of targets for modulation. Here, we report the identification of columbamine (COL) which enhances macrophage-mediated efferocytosis and attenuates intestinal inflammation in a murine colitis model. COL enhances efferocytosis by promoting LC3-associated phagocytosis (LAP), a non-canonical form of autophagy. Transcriptome analysis and pharmacological characterization revealed that COL is a biased agonist that occupies a part of the ligand binding pocket of formyl peptide receptor 2 (FPR2), a G-protein coupled receptor involved in inflammation regulation. Genetic ablation of the Fpr2 gene or treatment with an FPR2 antagonist abolishes COL-induced efferocytosis, anti-colitis activity and LAP. Taken together, our study identifies FPR2 as a potential target for modulating LC3-associated efferocytosis to alleviate intestinal inflammation and highlights the therapeutic value of COL, a natural and biased agonist of FPR2, in the treatment of inflammatory bowel disease.
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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 Socratic graph.