Angiogenesis articles from across Nature Portfolio

Myocardial infarction can damage the heart muscle and lead to heart failure. Research on recovery typically focuses on infiltrating immune cells, damaged cardiomyocytes, over-stimulated fibroblasts and changes in vasculature. Haykin et al. now describe a multi-organ circuit linking these entities, including the brain and liver, in the repair process.

Although epidermal growth factor-like domain 7 (Egfl7) is known to play a pro-angiogenic role in zebrafish, its contribution to brain lymphangiogenesis remains less clear. Here, the authors demonstrate that Egfl7 is dispensable for brain lymphatic endothelial cell specification, but not their migration and proliferation.

Haykin et al. show that activation of the brain’s reward system modulates adrenergic input to the liver and complement component 3 transcription, affecting vascularization and improving cardiac recovery after acute myocardial infarction.

This study reports a unexpected role in endothelial cells (ECs) for PCK2 in proteostasis, independent of its gluconeogenic activity. Perturbation of this role likely contributed to the angiogenic defects observed in ECs with reduced PCK2 levels.

Myocardial infarction can damage the heart muscle and lead to heart failure. Research on recovery typically focuses on infiltrating immune cells, damaged cardiomyocytes, over-stimulated fibroblasts and changes in vasculature. Haykin et al. now describe a multi-organ circuit linking these entities, including the brain and liver, in the repair process.

In this Tools of the Trade article, Berkeley and Thomson describe the use of a minimally invasive strategy to standardize the induction of myocardial infarction in mice.

Corey McAleese describes the study that identified the presence of metabolic heterogeneity in endothelial cells from different tissues and discusses its relevance to our current understanding of endothelial metabolism.

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.