Journal September 25, 2026 6 min read

How is angiogenesis measured?

Angiogenesis is quantified with endothelial tube-formation assays, gene and protein profiling of angiogenic mediators, and lesion-size or vessel-ingrowth endpoints in animal models.

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Angiogenesis is measured by combining functional endothelial assays with molecular readouts of angiogenic mediators and, in animal work, direct quantification of new vessel growth. The most common in vitro functional endpoint is the endothelial tube formation assay, in which endothelial cells are seeded on a matrix and the resulting capillary-like networks are counted; this is paired with targeted gene expression analysis and array-based profiling of angiogenesis-related proteins [4]. In vivo, angiogenesis is measured as lesion size or vessel ingrowth: laser-induced choroidal neovascularization (CNV) in C57BL/6J mice is quantified on RPE/choroid flat mounts, with immunostaining for myeloid cell accumulation and fibrosis-associated remodeling [5], while in vascular graft work the endpoints are adventitia ingrowth and endothelialization [8].

The pathway families that recur across this work are the VEGF axis and its receptor signaling, together with the NF-κB/IL-6 inflammatory arm and the PI3K-Akt-mTOR, MAPK and JAK-STAT cascades that feed into angiogenic gene expression [2][6][9].

Research Studies

Platelet-released growth factors and endothelial tube formation in vitro

Platelet-Released Growth Factors (PRGF) are a standardized, cell- and fibrin-free platelet lysate. In an endothelial cell-based model, PRGF were reported to exert pro-angiogenic effects at a working concentration of 10%, assessed by targeted gene expression analysis, array-based profiling of angiogenesis-related proteins, and functional endothelial tube formation assays [4]. The authors describe this as the first in vitro study of its kind for PRGF, and the findings are screening-level transcriptional and proteomic profiling in cultured endothelial cells rather than an in vivo measurement [4].

Nicotinamide mononucleotide and laser-induced choroidal neovascularization in mice

In a laser-induced CNV model in C57BL/6J mice, nicotinamide mononucleotide (NMN) was evaluated for its capacity to modulate the neurovascular inflammatory microenvironment and blunt tissue remodeling. CNV lesion size was quantified on RPE/choroid flat mounts, and immunostaining was used to assess myeloid cell accumulation and fibrosis-associated remodeling; quantitative RT-PCR and Western blotting assessed inflammatory and angiogenic gene expression and signaling activation in retina and RPE/choroid [5]. In vitro, LPS-stimulated bEnd.3 cells were used alongside the animal model [5]. These are animal and cell-culture findings.

Metformin and adventitia ingrowth in electrospun vascular grafts

Small-diameter vascular grafts require rapid endothelialization to maintain patency, and conventional surface modification provides limited biochemical signals for recruiting circulating endothelial cells. Three-dimensional minichannel-wrapped vascular grafts loaded with metformin were fabricated and tested on the hypothesis that perivascular pharmacological administration would promote adventitia ingrowth and accelerate fallout endothelialization [8]. The measured endpoints were adventitia ingrowth and endothelialization, with perivascular scarring and fibrosis as the problem being addressed [8].

Gemcitabine with ivonescimab and VEGF-pathway blockade in advanced NSCLC

A Phase II trial is investigating gemcitabine combined with ivonescimab, a bispecific PD-1/VEGF antibody, in patients with advanced non-small cell lung cancer who progressed after chemoimmunotherapy. Gemcitabine has shown immunostimulatory properties including enhanced T-cell infiltration and reduced immunosuppressive cell populations, and ivonescimab targets both PD-1 and VEGF pathways [2]. Angiogenesis here is engaged through the VEGF arm of a bispecific agent rather than measured as a standalone endpoint.

Ivosidenib, mFOLFOXIRI and celecoxib in BRAF V600E-mutant colorectal cancer

BRAF V600E-mutant colorectal cancer accounts for roughly 5–10% of colorectal cancer cases and is associated with aggressive progression and poor prognosis, particularly in metastatic settings; after first- and second-line treatment the median overall survival of patients is typically less than 24 months [3]. Anti-PD-1 therapies show limited efficacy in microsatellite-stable colorectal cancer but may hold promise in combination [3]. This trial combines ivosidenib with mFOLFOXIRI and celecoxib in BRAF-targeted-therapy-refractory disease [3].

Insulin resistance and angiogenic signaling in the tumor microenvironment

Insulin resistance contributes to hyperinsulinemia, disruption of insulin-like growth factor signaling, chronic inflammation and metabolic remodeling, producing a pro-tumorigenic milieu. These changes stimulate the PI3K-Akt-mTOR, MAPK, JAK-STAT and NF-κB pathways, which increase proliferation, survival, angiogenesis, immune escape and metastasis, and insulin resistance also modifies the tumor microenvironment and dampens anti-tumor immunity [6]. Monoclonal antibodies against IGF-1R, IL-6, IL-1β, TNF-α, PD-1, PD-L1 and CTLA-4 are discussed as candidate interventions in this setting [6].

2-deoxy-D-ribose and thymidine phosphorylase in the tumor microenvironment

Oncogenic drivers can elevate 2-deoxy-D-ribose (2dDR) levels by directing carbon flux toward the pentose phosphate pathway and nucleotide biosynthesis, increasing substrate availability for nucleoside phosphorylases, particularly thymidine phosphorylase (TP) as the primary enzymatic source of 2dDR [7]. The mechanisms uniquely linking TP overexpression to 2dDR accumulation in cancer remain poorly understood [7].

Senescence-associated secretory phenotype and tumor microenvironment remodeling

Cellular senescence influences cancer progression through irreversible cell-cycle arrest, immune surveillance and paracrine signaling mediated by the senescence-associated secretory phenotype (SASP). SASP comprises inflammatory cytokines, chemokines, growth factors and matrix-remodeling enzymes that regulate the tumor microenvironment [1]. This is a review of mechanisms of SASP induction, its condition-dependent roles in cancer, microenvironment remodeling, and strategies targeting senescent cells and SASP signaling [1].

Cathelicidin LL-37 and NF-κB/IL-6 signaling in gastric cancer

Cathelicidin LL-37, an antimicrobial peptide with context-dependent roles in cancer progression, was reported to inhibit angiogenesis and migration in gastric cancer via inhibition of NF-κB/IL-6 signaling [9].

Adipokines, endothelial dysfunction and preeclampsia

Adipokines are bioactive peptides secreted by adipose tissue that may contribute to the pathogenesis of preeclampsia through mechanisms involving inflammation, angiogenesis and endothelial dysfunction [10]. Separately, endothelial cells exposed to preeclamptic placental macrophages showed increased oxidative stress and impaired angiogenesis in vitro [12].

Comparison of representative angiogenesis measurement approaches

Approach	What is measured	Setting	Source
Endothelial tube formation assay	Capillary-like network formation by endothelial cells	In vitro	[4]
Angiogenesis protein array and targeted gene expression	Levels of angiogenesis-related transcripts and proteins	In vitro	[4]
CNV lesion size on RPE/choroid flat mounts	Lesion area; myeloid accumulation; fibrosis	Mouse (C57BL/6J)	[5]
Adventitia ingrowth and endothelialization	Vessel wall cellular ingrowth	Graft model	[8]
VEGF-pathway engagement via bispecific antibody	PD-1 and VEGF pathway targeting	Human trial (NSCLC)	[2]

Transcriptomic profiling in T-cell lymphomas

An integrative pooled transcriptomic analysis compared adult T-cell leukemia/lymphoma, which originates from HTLV-1 infection, with peripheral T-cell lymphomas, a heterogeneous group without a defined etiologic factor, to identify shared and distinct molecular signatures [11].

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