Journal September 25, 2026 7 min read

What is angiogenesis?

Angiogenesis is the formation of new blood vessels from pre-existing vasculature, driven by endothelial cell activation, proliferation, migration and tube formation. This page summarises laboratory and clinical research

peptides-pro Editorial

Angiogenesis is the process by which new blood vessels form from pre-existing vasculature. It is distinct from vasculogenesis, which describes de novo vessel formation from endothelial progenitor cells. The term is used across developmental biology, oncology, wound healing and regenerative medicine, and the process is studied chiefly in endothelial cell models, animal models and human clinical trials. No single molecular formula or sequence defines angiogenesis; it is a process, not a compound, and the identifiers that appear in the literature belong to the individual mediators and inhibitors studied.

The work described below centres on several signalling families, including vascular endothelial growth factor (VEGF) and its receptors, the platelet-derived growth factor (PDGF) family, angiopoietin–Tie signalling, and the NF-κB/IL-6 inflammatory axis, with additional input from metabolic and senescence-associated pathways.

Research Studies

Platelet-released growth factors and pro-angiogenic effects in endothelial cells

Platelet-Released Growth Factors (PRGF) are a standardised, cell- and fibrin-free platelet lysate studied for tissue repair. In an in vitro endothelial cell model, PRGF were reported to exert pro-angiogenic effects at a working concentration of 10%. The study combined targeted gene expression analysis, array-based profiling of angiogenesis-related proteins, and functional endothelial tube formation assays. The authors describe this as the first in vitro study of its kind for PRGF and frame the findings in the context of wound healing and regenerative medicine, where angiogenesis is required to restore perfusion in chronic and non-healing wounds [4].

Nicotinamide mononucleotide and choroidal neovascularisation in a mouse model

Nicotinamide mononucleotide (NMN) was evaluated for its capacity to modulate the neurovascular inflammatory microenvironment and blunt tissue remodelling in neovascular age-related macular degeneration (nAMD). A laser-induced choroidal neovascularisation (CNV) model was established in C57BL/6J mice, with lesion size quantified on RPE/choroid flat mounts. Immunostaining was used to assess myeloid cell accumulation and fibrosis-associated remodelling, and quantitative RT-PCR and Western blotting assessed inflammatory and angiogenic gene expression and signalling activation in retina and RPE/choroid. In vitro work used lipopolysaccharide-stimulated bEnd.3 cells [5]. These findings are animal-model and in vitro observations.

Metformin and perivascular administration in electrospun vascular grafts

Rapid endothelialisation is a persistent challenge for small-diameter vascular grafts. In work using three-dimensional minichannel-wrapped electrospun grafts loaded with metformin, perivascular administration was hypothesised to promote adventitia ingrowth and accelerate fallout endothelialisation. The rationale cited was that regenerated adventitia facilitates endothelialisation, and that conventional surface modification provides limited biochemical signals for recruiting circulating endothelial cells while failing to mitigate perivascular scarring and fibrosis [8]. This is a preclinical graft study.

Senescence-associated secretory phenotype and tumour microenvironment remodelling

Cellular senescence influences cancer progression through irreversible cell-cycle arrest, immune surveillance and paracrine signalling mediated by the senescence-associated secretory phenotype (SASP). SASP comprises inflammatory cytokines, chemokines, growth factors and matrix-remodelling enzymes that regulate the tumour microenvironment. A review describes current evidence on SASP induction mechanisms, its condition-dependent roles in cancer, tumour microenvironment remodelling, and emerging strategies targeting senescent cells and SASP signalling [1]. Angiogenesis is one of the processes influenced by this secretory programme.

Insulin resistance and angiogenic signalling in cancer

Insulin resistance (IR) is implicated in the development, progression and treatment resistance of cancer. Beyond its contribution to obesity and type 2 diabetes, IR leads to hyperinsulinaemia, disruption of insulin-like growth factor signalling, chronic inflammation and metabolic remodelling, 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. IR also modifies the tumour microenvironment and dampens anti-tumour immunity. Monoclonal antibodies against IGF-1R, IL-6, IL-1β, TNF-α, PD-1, PD-L1 and CTLA-4 are discussed as candidate interventions [6].

2-deoxy-D-ribose and metabolic control of the tumour microenvironment

2-deoxy-D-ribose (2dDR) has emerged as a metabolite shaping the tumour microenvironment. Oncogenic drivers can elevate 2dDR levels by directing carbon flux toward the pentose phosphate pathway and nucleotide biosynthesis, increasing substrate availability for nucleoside phosphorylases, particularly thymidine phosphorylase (TP), described as the primary enzymatic source of 2dDR. The mechanisms uniquely linking TP overexpression to 2dDR accumulation in cancer remain poorly understood [7]. Thymidine phosphorylase is itself a known angiogenic mediator, which places 2dDR at the crossroads of cancer metabolism and vessel formation.

Gemcitabine with ivonescimab in advanced NSCLC

A Phase II clinical trial is investigating the combination of gemcitabine, a chemotherapy agent, with ivonescimab, a bispecific PD-1/VEGF antibody, in patients with advanced non-small cell lung cancer (NSCLC) who have progressed after chemoimmunotherapy. Gemcitabine has demonstrated immunostimulatory properties, including enhanced T-cell infiltration and reduced immunosuppressive cell populations, which may synergise with immune checkpoint inhibitors. Ivonescimab targets both PD-1 and VEGF pathways [2]. VEGF pathway targeting is directly relevant to angiogenic signalling in tumours.

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

BRAF-mutated colorectal cancer, driven primarily by the BRAF V600E mutation, accounts for approximately 5–10% of all colorectal cancer cases and is associated with aggressive progression and poor prognosis, particularly in metastatic settings. After first- and second-line treatments, median overall survival is typically less than 24 months, and progression is rapid once resistance develops. Immune checkpoint inhibitors such as anti-PD-1 therapies show limited efficacy in microsatellite-stable colorectal cancers but may hold promise in combination with other agents [3]. The trial combines ivosidenib, mFOLFOXIRI and celecoxib in this population.

Cathelicidin LL-37 and inhibition of angiogenesis in gastric cancer

Cathelicidin LL-37, an antimicrobial peptide with context-dependent roles in cancer progression, has been reported to inhibit angiogenesis and migration in gastric cancer via inhibition of NF-κB/IL-6 signalling [9]. This is a reference-only finding and is reported here as a fact of the literature rather than as the focus of this page.

Adipokines, preeclampsia and endothelial dysfunction

Preeclampsia is a multifactorial hypertensive disorder of pregnancy. Adipokines — bioactive peptides secreted by adipose tissue — may contribute to its pathogenesis through mechanisms involving inflammation, angiogenesis and endothelial dysfunction [10]. Related in vitro work reports that endothelial cells exposed to preeclamptic placental macrophages show increased oxidative stress and impaired angiogenesis [12]. These are reference-only findings.

Comparative transcriptomic signatures in T-cell lymphomas

Adult T-cell leukemia/lymphoma (ATLL) and peripheral T-cell lymphomas (PTCLs) are aggressive neoplasms of mature T cells with poor prognosis and limited therapies. ATLL originates from HTLV-1 infection, while PTCL comprises heterogeneous subtypes without a defined etiologic factor. Comparative molecular profiling of these entities has been undertaken in pooled transcriptomic analyses [11]. This is a reference-only finding.

Comparison of selected angiogenesis-related study contexts

Agent or mediator	Model or population	Angiogenesis-related observation
Platelet-Released Growth Factors (PRGF)	In vitro endothelial cell model	Pro-angiogenic effects at 10% working concentration; tube formation supported [4]
Nicotinamide mononucleotide (NMN)	Laser-induced CNV in C57BL/6J mice; LPS-stimulated bEnd.3 cells in vitro	Attenuation of inflammatory activation, choroidal neovascularisation and lesion-associated remodelling [5]
Metformin	Electrospun vascular grafts, perivascular administration	Improved adventitia ingrowth and endothelialisation [8]
Ivonescimab (PD-1/VEGF bispecific)	Phase II trial, advanced NSCLC after chemoimmunotherapy	Dual PD-1 and VEGF pathway targeting [2]
Cathelicidin LL-37	Gastric cancer (reference-only)	Inhibition of angiogenesis and migration via NF-κB/IL-6 [9]

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