ArticleEMBO molecular medicine2013
PHD2 regulates arteriogenic macrophages through TIE2 signalling.
Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
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- Single-cell compendium of muscle microenvironment in peripheral artery disease reveals altered endothelial diversity and LYVE1Nature cardiovascular research · 2025Article
- Macrophage regulation of tumor cell dormancy and the dormant niche: an overview in solid tumors.Cancer metastasis reviews · 2025Review
- Generation of Phd2-haplodeficient macrophages with proresolution effects for the treatment of limb ischemia.Frontiers in pharmacology · 2025Article
- The Immune-Centric Revolution Translated into Clinical Application: Peripheral Blood Mononuclear Cell (PBMNC) Therapy in Diabetic Patients with No-Option Critical Limb-Threatening Ischemia (NO-CLTI)-Rationale and Meta-Analysis of Observational Studies.Journal of clinical medicine · 2024Review
- HTATIP2 regulates arteriogenic activity in monocytes from patients with limb ischemia.JCI insight · 2023Article
- Review
- Monocyte proinflammatory phenotypic control by ephrin type A receptor 4 mediates neural tissue damage.JCI insight · 2022Article
- Tie2-expressing monocytes/macrophages promote cerebral revascularization in peri-infarct lesions upon ischemic insult.Signal transduction and targeted therapy · 2021Article
- Dual delivery of IL-10 and AT-RvD1 from PEG hydrogels polarize immune cells towards pro-regenerative phenotypes.Biomaterials · 2021Article
- The Role of Macrophages in Vascular Repair and Regeneration after Ischemic Injury.International journal of molecular sciences · 2020Review
- Tooth Regeneration: Insights from Tooth Development and Spatial-Temporal Control of Bioactive Drug Release.Stem cell reviews and reports · 2020Review
- Acute and chronic hypoxia differentially predispose lungs for metastases.Scientific reports · 2019Article
- Angiopoietin 1 influences ischemic reperfusion renal injury via modulating endothelium survival and regeneration.Molecular medicine (Cambridge, Mass.) · 2019Article
- Regulation of Blood and Lymphatic Vessels by Immune Cells in Tumors and Metastasis.Annual review of physiology · 2019Review
- Dual Affinity Heparin-Based Hydrogels Achieve Pro-Regenerative Immunomodulation and Microvascular Remodeling.ACS biomaterials science & engineering · 2018Article
- Article
- Elementary immunology: NaPediatric nephrology (Berlin, Germany) · 2017Review
- CD40 in coronary artery disease: a matter of macrophages?Basic research in cardiology · 2016Review
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Authors and funding
15 authors at 6 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Occlusion of the main arterial route redirects blood flow to the collateral circulation. We previously reported that macrophages genetically modified to express low levels of prolyl hydroxylase domain protein 2 (PHD2) display an arteriogenic phenotype, which promotes the formation of collateral vessels and protects the skeletal muscle from ischaemic necrosis. However, the molecular mechanisms underlying this process are unknown. Here, we demonstrate that femoral artery occlusion induces a switch in macrophage phenotype through angiopoietin-1 (ANG1)-mediated Phd2 repression. ANG blockade by a soluble trap prevented the downregulation of Phd2 expression in macrophages and their phenotypic switch, thus inhibiting collateral growth. ANG1-dependent Phd2 repression initiated a feed-forward loop mediated by the induction of the ANG receptor TIE2 in macrophages. Gene silencing and cell depletion strategies demonstrate that TIE2 induction in macrophages is required to promote their proarteriogenic functions, enabling collateral vessel formation following arterial obstruction. These results indicate an indispensable role for TIE2 in sustaining in situ programming of macrophages to a proarteriogenic, M2-like phenotype, suggesting possible new venues for the treatment of ischaemic disorders.
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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.