Macrophage skewing by Phd2 haplodeficiency prevents ischaemia by inducing arteriogenesis.

doi:10.1038/nature10507

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Macrophage skewing by Phd2 haplodeficiency prevents ischaemia by inducing arteriogenesis.

Nature - 9 Oct 2011

Takeda Yukiji, Costa Sandra, Delamarre Estelle, Roncal Carmen, Leite de Oliveira Rodrigo, Squadrito Mario Leonardo, Finisguerra Veronica, Deschoemaeker Sofie, Bruyère Françoise, Wenes Mathias, Hamm Alexander, Serneels Jens, Magat Julie, Bhattacharyya Tapan, Anisimov Andrey, Jordan Benedicte F, Alitalo Kari, Maxwell Patrick, Gallez Bernard, Zhuang Zhen W, Saito Yoshihiko, Simons Michael, De Palma Michele, Mazzone Massimiliano

Abstract excerpt

PHD2 serves as an oxygen sensor that rescues blood supply by regulating vessel formation and shape in case of oxygen shortage. However, it is unknown whether PHD2 can influence arteriogenesis. Here we studied the role of PHD2 in collateral artery growth by using hindlimb ischaemia as a model, a process that compensates for the lack of blood flow in case of major arterial occlusion. We show that Phd2 (also known...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Arteries

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Extremities

Share to Hypoxia-Inducible Factor-Proline Dioxygenases

Share to Ischemia

Share to Mice, 129 Strain

Share to Myocytes, Smooth Muscle

Share to Necrosis

Share to Procollagen-Proline Dioxygenase

Source

Open in PubMed Open full text

Identifiers

PMID: 21983962
DOI: 10.1038/nature10507
PMCID: PMC4659699

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Macrophage skewing by Phd2 haplodeficiency prevents ischaemia by inducing arteriogenesis.PMID 21983962Read ↗

PHD2 regulates arteriogenic macrophages through TIE2 signalling.Semantic proximity Read ↗

Blood vessel control of macrophage maturation promotes arteriogenesis in ischemia.Semantic proximity Read ↗

ApoA-I Nanotherapy Rescues Postischemic Vascular Maladaptation by Modulating Endothelial Cell and Macrophage Phenotypes in Type 2 Diabetic Mice.Semantic proximity Read ↗

Myeloid Drp1 Deficiency Limits Revascularization in Ischemic Muscles via Inflammatory Macrophage Polarization and Metabolic ReprogramingSemantic proximity Read ↗

Essential role for prolyl hydroxylase domain protein 2 in oxygen homeostasis of the adult vascular system.Semantic proximity Read ↗

Murine limb ischaemia induces structural and functional remodelling of local and distant bone marrowSemantic proximity Read ↗

AMP-Activated Protein Kinase α1 in Macrophages Promotes Collateral Remodeling and Arteriogenesis in Mice In Vivo.Semantic proximity Read ↗

Deletion or Inhibition of the Oxygen Sensor PHD1 Protects against Ischemic Stroke via Reprogramming of Neuronal Metabolism.Semantic proximity Read ↗

The temporal and spatial distribution of macrophage subpopulations during arteriogenesis.Semantic proximity Read ↗

Role of macrophage-derived hypoxia-inducible factor (HIF)-1α as a mediator of vascular remodelling.Semantic proximity Read ↗

Myeloid DRP1 Sulfenylation Drives Reparative Macrophage Polarization and Neovascularization in Ischemic MuscleSemantic proximity Read ↗

HIMF deletion ameliorates acute myocardial ischemic injury by promoting macrophage transformation to reparative subtype.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.