Angiogenesis articles from across Nature Portfolio

Organs develop unique vascular architectures to support physiological functions. Here, authors show that organo-typical vascular networks may arise from specific parenchymal cues activating unique endothelial subtypes and angiogenic sprouting processes.

Arteries are vital blood vessels for our body and their growth and patterning are critical for proper blood flow. Here they use a retina model to show that a balance of EphB4 receptor and ephrin-B2 ligand integrate a well-wired molecular network to control arteriovenous patterning and vascular growth.

A molecular mechanism for brain-specific angiogenesis operates under the control of Wnt7a/b ligands.

Osteocytes are the key cellular components of cortical bone. Here they show that osteocytes transfer mitochondria to the endothelial cells of transcortical vessels (TCVs), which promotes angiogenesis and increases function of the TCV network.

The intracellular effectors of bone morphogenetic protein signaling, SMAD1/5, act in skeleton-resident endothelial cells to direct bone formation in long bones of juvenile mice.

Myocardial infarction causes endoplasmic reticulum (ER) stress, thereby triggering the release of a set of poorly defined growth factors. A study shows that the growth factor CRELD2 is secreted in response to ER stress and is required for preserving heart function after myocardial infarction in mice.

In acute myocardial infarction treated with reperfusion, functional preservation of myocardium requires an angiogenic response. A new study shows that CRELD2, an endoplasmic reticulum (ER)-resident protein induced in response to ER stress, acts as an angiocrine factor to limit cardiac dysfunction after ischemia/reperfusion injury in mice.

Bone marrow endothelial cells deliver oxygen and nutrients and regulate bone formation and haematopoiesis in the surrounding microenvironment. A new study identifies a subtype of capillary that occurs exclusively in the epiphysis and displays unique characteristics that have a role in balancing osteogenesis and haematopoiesis.

Vascular patterning is dictated by transcription factors, such as the Notch pathway. Molecular profiling has uncovered snapshots of the transcriptional specification of endothelial cell tubulogenesis. Here, the authors leverage the output of Notch signaling, demonstrating that vascular remodeling is poorly predicted by transcriptional profiling.

We report an intronic variant of the endothelial angiopoietin receptor TIE2 that is associated with increased gene expression and decreased risk of coronary artery disease. Genetic deletion of Tie2 in hypercholesterolemic mice shows that the Tie2 receptor protects from atherosclerosis by controlling inflammation in the arterial wall.