The reason for this cross-disciplinary reach is simple: blood vessels are everywhere, and when they misbehave, disease follows. Tumor angiogenesis is now recognized as a hallmark of cancer, enabling tumor growth, metastasis, and immune evasion. In the eye, pathological neovascularization remains a leading cause of blindness worldwide through diabetic retinopathy. In cardiovascular and peripheral artery disease, the failure to mount an adequate angiogenic response underlies tissue ischemia, starving limbs and heart muscle of oxygen. Chronic respiratory conditions, from chronic obstructive pulmonary disease to pulmonary hypertension and lung cancer, are increasingly understood as diseases of vascular remodeling. Even gynecological disorders such as endometriosis and adenomyosis depend heavily on new vessel formation, and inhibiting that process can suppress disease progression. The COVID-19 pandemic added yet another dimension, revealing SARS-CoV-2 infection as fundamentally a vascular pathology in which endothelial activation and angiogenic dysregulation predicted severity and mortality.

This cross-disease relevance is precisely what makes the field so consequential. A discovery about endothelial cell metabolism in tumors can inform vascular normalization strategies that improve the delivery of cancer immunotherapy. A finding about how microglia, the resident immune cells of the retina, regulate retinal angiogenesis can open therapeutic avenues for diabetic eye disease. The work published in the vascular biology literature resonates far beyond the community that produced it, feeding directly into clinical decisions made by oncologists, ophthalmologists, cardiologists, and pulmonologists. The most highly cited articles from the past two years illustrate this scope with striking clarity, spanning tumor biology, ophthalmology, regenerative medicine, respiratory disease, and methodological innovation.

In ocular angiogenesis, one of the most cited recent works provided a comprehensive review of microglial regulation of retinal angiogenesis and its role in diabetic retinopathy, a condition that threatens the sight of hundreds of millions of people with diabetes. Complementing that effort, researchers demonstrated that apolipoprotein M-bound sphingosine-1-phosphate acts through the endothelial receptor S1PR1 to suppress choroidal neovascularization and vascular leakage. The finding is significant because it suggests a potential systemic alternative to the repeated intraocular anti-VEGF injections that patients with neovascular age-related macular degeneration must currently endure, offering hope for a less burdensome treatment paradigm for the leading cause of vision loss in older adults.

Tumor vascular biology has been equally productive. A major review of the therapeutic landscape of tumor angiogenesis focused particular attention on how infiltrating myeloid cells, including macrophages, myeloid-derived suppressor cells, and neutrophils, regulate vascular remodeling and drive resistance to therapy. This line of inquiry matters because anti-angiogenic drugs, while clinically validated, often fail or lose effectiveness as tumors recruit their own inflammatory support systems. Another team highlighted Group XIV C-type lectins as emerging targets in tumor angiogenesis, identifying proteins such as CD93 and thrombomodulin as drivers of pathological neovascularization and metastatic spread. In a separate mechanistic study, investigators identified the endothelial G protein-coupled receptor GPR182 as a negative regulator of sprouting angiogenesis that acts by modulating the CXCL12-CXCR4 signaling axis, an observation with direct implications for hepatocellular carcinoma, a cancer notoriously resistant to existing treatments.

Regenerative medicine represents the other face of angiogenesis research: instead of blocking vessel growth, clinicians want to encourage it where tissue is starved of blood supply. A review of cord blood-derived endothelial colony-forming cells examined their immune-privileged properties and their promise for allogeneic cytotherapy and tissue engineering, potentially allowing off-the-shelf vascular cell therapies that the body will not reject. Even more striking was a preclinical study in which researchers developed an SDF-1alpha messenger RNA therapy delivered via lipid nanoparticles, the same platform technology that proved itself in COVID-19 vaccines, and accelerated blood flow recovery in a mouse model of hindlimb ischemia. For patients with peripheral artery disease and critical limb ischemia, who today face amputation when bypass and stenting fail, such therapeutic angiogenesis strategies represent a genuine lifeline in development.

Respiratory vascular biology has emerged as one of the fastest-moving subfields. An authoritative review mapped the role of the vasculature and angiogenesis across both non-neoplastic and neoplastic lung diseases, from infection and COPD to pulmonary fibrosis, pulmonary hypertension, and lung cancer, arguing that vascular changes are not secondary consequences of lung disease but active drivers of progression. Another detailed review tackled soluble FLT-1, the soluble form of the VEGF receptor 1, tracing its discovery, the splicing mechanisms that generate it, its prevalence across diseases, and its therapeutic applications as a natural neutralizer of vascular endothelial growth factor. On the methods front, researchers introduced a novel quantitative angiogenesis assay based on visualized vascular organoids, giving the community a standardized tool for measuring neovascularization in three-dimensional human tissue models rather than relying on less predictive animal or two-dimensional assays.

Behind this scientific flowering lies a sobering policy argument that the journal’s editors make explicitly: the progress reflected in these pages is the product of sustained public investment in biomedical research, and that investment is now under threat. Across the United States and many partner nations, research budgets have stagnated, eroded by inflation and competing political priorities. Flat funding, the editors warn, is not neutral; it is a slow disinvestment. It means promising grants go unfunded, early-career scientists leave the field, and laboratories that should be pursuing the next breakthrough are instead scaling back. The editors call for pressure on Congress and elected representatives to increase federal research appropriations, arguing that the return on this investment is concrete rather than abstract.

The clinical dividends of that investment are already visible. Anti-angiogenic therapies extend lives in metastatic colorectal cancer, renal cell carcinoma, and hepatocellular carcinoma. VEGF inhibitors preserve vision in millions of patients with macular degeneration and diabetic retinopathy. Therapeutic angiogenesis strategies hold promise for patients with critical limb ischemia who have no other options. Every one of these advances, the editors note, traces back to federally funded basic research on endothelial cell biology, work that cannot be sustained by private investment alone because its payoffs are too long-term and too fundamental. Biomedical research funding, they argue, should be understood not as discretionary spending but as an investment in public health, economic competitiveness, and national scientific leadership.

The journal’s new impact factor also reflects the health of its scholarly community. The editors credit an editorial board whose expertise and judgment ensure rigorous and fair evaluation, and a large, growing group of volunteer peer reviewers whose collective effort allows a median time to first decision of approximately five days without compromising scientific quality. Looking forward, the journal has invited submissions across the full spectrum of angiogenesis science, from basic mechanisms of endothelial cell heterogeneity and plasticity to novel therapeutic strategies and clinical investigations. If the past two years are any guide, that spectrum will only widen, as the vessels that feed our tissues continue to reveal new molecular levers for treating cancer, blindness, ischemia, and inflammatory disease alike. The field, as its title suggests, is indeed in full bloom, and its fruits are reaching the clinic faster than ever before.

Subject of Research: Mechanisms and therapeutic targeting of blood vessel formation in health and disease

Article Title: Angiogenesis: a research field in full bloom

Article References: Dudley, A. C., & Griffioen, A. W. (2026). Angiogenesis: a research field in full bloom. Angiogenesis, 29(4), Article 76. https://doi.org/10.1007/s10456-026-10077-1

Image Credits: AI Generated

DOI: 10.1007/s10456-026-10077-1

Keywords: angiogenesis, vascular biology, tumor angiogenesis, VEGF, diabetic retinopathy, peripheral artery disease, endothelial cells, immunotherapy, organoids, biomedical research funding, macular degeneration, regenerative medicine