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Hedi Raizer

Journal 7 min read

What does the research say about angiogenesis?

Angiogenesis is the formation of new blood vessels from existing vasculature. This page summarises laboratory and clinical research on pro- and anti-angiogenic mechanisms, including in vitro endothelial models, animal mo

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. In the research literature, angiogenesis is studied as a multi-step process involving endothelial cell activation, basement membrane degradation, migration, proliferation, tube formation, and vessel stabilisation. The process is regulated by a balance of pro-angiogenic and anti-angiogenic signals, including vascular endothelial growth factor (VEGF), platelet-derived growth factors, angiopoietins, and inflammatory cytokines. No single molecular formula or sequence defines angiogenesis as a whole; it is a biological process rather than a discrete compound.

The work described on this page centres on VEGF signalling and its interaction with immune checkpoint pathways, alongside broader cytokine and growth factor networks such as NF-κB/IL-6 and PI3K-Akt-mTOR.

Research Studies

Platelet-released growth factors and endothelial tube formation in vitro

Platelet-Released Growth Factors (PRGF) are described as a standardized, cell- and fibrin-free platelet lysate. In an in vitro study using an endothelial cell-based model, PRGF were reported to exert pro-angiogenic effects at a working concentration of 10%. The study integrated targeted gene expression analysis, array-based profiling of angiogenesis-related proteins, and functional endothelial tube formation assays. The authors present this as the first in vitro study demonstrating these effects for PRGF in this model system [4].

This evidence is in vitro only. It does not establish whether the same effects occur in animals or humans.

Nicotinamide mononucleotide and choroidal neovascularization in mice

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

This evidence is animal and in vitro only. No human dosing or clinical outcome data are provided in the evidence block.

Metformin and endothelialization of vascular grafts in a preclinical model

Perivascular administration of metformin through 3D minichannels was investigated for its effect on adventitia ingrowth and endothelialization in electrospinning vascular grafts. The study rationale was that pharmacological administration around vascular grafts could promote rapid adventitia ingrowth and accelerate fallout endothelialization. Three-dimensional minichannel-wrapped vascular grafts loaded with metformin were fabricated and tested [8].

This evidence is preclinical. It does not establish clinical benefit in humans.

Ivonescimab, gemcitabine, and VEGF/PD-1 pathways in advanced NSCLC

A Phase II clinical trial is investigating the efficacy of combining gemcitabine, a chemotherapy agent, with ivonescimab, a bispecific PD-1/VEGF antibody, in patients with advanced non-small cell lung cancer (NSCLC) who have experienced disease progression following chemoimmunotherapy (CIT). Gemcitabine has demonstrated immunostimulatory properties, including enhanced T-cell infiltration and reduced immunosuppressive cell populations, which may synergize with immune checkpoint inhibitors. Ivonescimab targets both PD-1 and VEGF pathways [2].

This is an ongoing clinical trial. Results are not yet available in the evidence block.

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

BRAF-mutated colorectal cancer, primarily driven by the BRAF V600E mutation, accounts for approximately 5–10% of all colorectal cancer cases and is associated with aggressive disease progression and poor prognosis, particularly in metastatic settings. Following first- and second-line treatments, including chemotherapy and targeted therapy, the median overall survival of patients is typically less than 24 months, and tumour progression is rapid once resistance develops. A clinical trial is investigating ivosidenib plus mFOLFOXIRI and celecoxib in this population. Previous studies have demonstrated that immune checkpoint inhibitors, such as anti-PD-1 therapies, show limited efficacy in microsatellite-stable (MSS) colorectal cancers but may hold promise when combined with other agents [3].

This is an ongoing clinical trial. Angiogenesis-related outcomes are not specified in the evidence block.

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 (TME). A review describes the current evidence on the mechanisms of SASP induction, its condition-dependent roles in cancer, TME remodelling, and emerging strategies targeting senescent cells and SASP signalling [1].

This is a review of preclinical and clinical literature. It does not report a new primary study.

Insulin resistance and angiogenic signalling in cancer

Insulin resistance (IR) is involved in the development, progression, and treatment resistance of cancer. IR leads to hyperinsulinaemia, disruption of insulin-like growth factor signalling, chronic inflammation, and metabolic remodelling, which fosters 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 (TME) and dampens anti-tumour immunity. IGF-1R, IL-6, IL-1β, TNF-α, PD-1, PD-L1, and CTLA-4 monoclonal antibodies could be beneficial by inhibiting inflammatory signalling [6].

This is a review. It synthesises preclinical and clinical findings but does not report a new primary study.

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

2-deoxy-D-ribose (2dDR) has emerged as a key metabolite shaping the tumour microenvironment (TME). Oncogenic drivers can elevate 2dDR levels by directing carbon flux toward the pentose phosphate pathway (PPP) and nucleotide biosynthesis. This increases substrate availability for nucleoside phosphorylases, particularly thymidine phosphorylase (TP), as the primary enzymatic source of 2dDR. However, the mechanisms uniquely linking TP overexpression to 2dDR accumulation in cancer remain poorly understood [7].

This is a review. It does not report a new primary study.

Cathelicidin LL-37 and angiogenesis in gastric cancer

Cathelicidin LL-37, an antimicrobial peptide, has demonstrated context-dependent roles in cancer progression. A study reports that LL-37 inhibits angiogenesis and migration in gastric cancer via inhibition of NF-κB/IL-6 signalling [9].

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Adipokines and angiogenesis in preeclampsia

Preeclampsia is a multifactorial hypertensive disorder of pregnancy with major clinical consequences. Adipokines—bioactive peptides secreted by adipose tissue—may contribute to its pathogenesis through mechanisms involving inflammation, angiogenesis, and endothelial dysfunction. A review summarises findings from various studies [10].

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Endothelial cells and preeclamptic placental macrophages in vitro

Preeclampsia (PE) is a hypertensive disorder of pregnancy characterised by endothelial dysfunction and immune dysregulation, with delivery remaining the only curative treatment. Although aberrant macrophage (MΦ) polarisation has been implicated in PE, the mechanisms by which placental MΦs contribute to endothelial dysfunction are not fully understood. A study reports that endothelial cells exposed to preeclamptic placental macrophages show increased oxidative stress and impaired angiogenesis in vitro [12].

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Integrative transcriptomic analysis 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. A comparative molecular profiling study reports shared and distinct molecular signatures in these conditions [11].

This is a reference-only item. It supports the page but is not its content.

If you are reading this for personal health reasons

The materials described on this page are sold for laboratory research only. We do not provide dosing or medical guidance. Anyone considering a compound for themselves should speak to a licensed clinician.

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