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Hedi Raizer

Journal 6 min read

Common Misconceptions About Angiogenesis

Angiogenesis is the formation of new blood vessels from pre-existing vasculature. This page examines what laboratory research does and does not show about its regulation, with evidence drawn from in vitro, animal, and cl

peptides-pro Editorial

Angiogenesis is the process by which new blood vessels arise from pre-existing vasculature. It is distinct from vasculogenesis, which refers to de novo vessel formation from endothelial progenitor cells. In the research literature, angiogenesis is studied across wound healing, cancer, ocular disease, and reproductive pathology. The process is governed by a balance of pro- and anti-angiogenic signals, and the vascular endothelial growth factor (VEGF) pathway is the most extensively characterised receptor family in this field.

Misconceptions about angiogenesis often arise when findings from one model system are generalised to another. A compound that promotes tube formation in cultured endothelial cells may not produce the same effect in a whole organism, and a mechanism observed in a mouse model may not translate to human tissue. The studies below illustrate this point.

Research Studies

Platelet-Released Growth Factors and Endothelial Tube Formation In Vitro

Platelet-Released Growth Factors (PRGF) are a standardised, cell- and fibrin-free platelet lysate. In an in vitro study using an endothelial cell-based model, PRGF at a working concentration of 10% were reported to exert pro-angiogenic effects. The study integrated targeted gene expression analysis, array-based profiling of angiogenesis-related proteins, and functional endothelial tube formation assays [5]. These findings are limited to the in vitro setting and do not establish that PRGF promote angiogenesis in vivo.

Nicotinamide Mononucleotide and Choroidal Neovascularization in Mice

Nicotinamide mononucleotide (NMN) was evaluated in a laser-induced choroidal neovascularization (CNV) model in C57BL/6J mice. CNV lesion size was quantified on RPE/choroid flat mounts, and immunostaining assessed myeloid cell accumulation and fibrosis-associated remodelling. In vitro, lipopolysaccharide-stimulated bEnd.3 cells were used to examine inflammatory and angiogenic gene expression [6]. The study reported that NMN attenuated inflammatory activation, choroidal neovascularization, and lesion-associated remodelling. These findings are animal- and in vitro-based; they do not establish efficacy in human neovascular age-related macular degeneration.

Zinc Silicate Microspheres and Bacterial Metabolic Interference in Chronic Wounds

Zinc silicate flower-like microspheres (ZnSi FMPs) were designed with a controlled hierarchical architecture for chronic wound repair. The nanosheet structure provides sustained Zn2+ release, and the material was reported to have pH-independent antibacterial activity. The proposed mechanism involves bacterial metabolic interference and microenvironment remodelling [1]. This work is presented as a novel multifaceted agent; the evidence does not establish that ZnSi FMPs directly promote angiogenesis in human chronic wounds.

Cathelicidin LL-37 and Angiogenesis in Gastric Cancer

Cathelicidin LL-37, an antimicrobial peptide, has demonstrated context-dependent roles in cancer progression. A study reported that LL-37 inhibits angiogenesis and migration in gastric cancer via inhibition of NF-κB/IL-6 signalling [9]. This finding is specific to the gastric cancer model studied and does not imply that LL-37 inhibits angiogenesis in all tissues or disease contexts.

Senescence-Associated Secretory Phenotype and Tumour Microenvironment Remodelling

The senescence-associated secretory phenotype (SASP) comprises inflammatory cytokines, chemokines, growth factors, and matrix-remodelling enzymes that regulate the tumour microenvironment. A review describes the current evidence on SASP induction, its condition-dependent roles in cancer, and emerging strategies targeting senescent cells and SASP signalling [2]. The review does not establish a single universal effect of SASP on angiogenesis; its role is described as condition-dependent.

Insulin Resistance and Angiogenesis in Cancer

Insulin resistance (IR) is involved in the development, progression, and treatment resistance of cancer. IR leads to hyperinsulinemia, disruption of insulin-like growth factor signalling, chronic inflammation, and metabolic remodelling. These changes stimulate the PI3K-Akt-mTOR, MAPK, JAK-STAT, and NF-κB pathways, which increase proliferation, survival, angiogenesis, immune escape, and metastasis [7]. This is a review-level synthesis; it does not report a primary experimental test of angiogenesis in a specific model.

2-Deoxy-D-Ribose and 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 thymidine phosphorylase (TP) [8]. The mechanisms uniquely linking TP overexpression to 2dDR accumulation in cancer remain poorly understood. This review does not establish that 2dDR directly regulates angiogenesis.

Adipokines and Angiogenesis in Preeclampsia

Preeclampsia is a multifactorial hypertensive disorder of pregnancy. Adipokines are bioactive peptides secreted by adipose tissue that may contribute to its pathogenesis through mechanisms involving inflammation, angiogenesis, and endothelial dysfunction [10]. This review summarises findings from various studies; it does not establish a causal role for any single adipokine in angiogenic regulation.

Endothelial Cells and Preeclamptic Placental Macrophages In Vitro

Endothelial cells exposed to preeclamptic placental macrophages show increased oxidative stress and impaired angiogenesis in vitro [12]. This finding is limited to the in vitro model used and does not establish that the same impairment occurs in vivo in human preeclampsia.

Comparison of Selected Findings

Agent or FactorModelReported Effect on Angiogenesis
PRGF (10%)In vitro endothelial cell modelPro-angiogenic effects [5]
NMNMouse laser-induced CNV; in vitro bEnd.3 cellsAttenuated choroidal neovascularization [6]
LL-37Gastric cancer modelInhibited angiogenesis and migration [9]
Preeclamptic placental macrophagesIn vitro endothelial cellsImpaired angiogenesis [12]

Clinical Trial Contexts Involving Angiogenesis-Related Pathways

Several clinical trials are investigating agents that target pathways with known roles in angiogenesis. A Phase II trial is evaluating gemcitabine combined with ivonescimab, a bispecific PD-1/VEGF antibody, in patients with advanced non-small cell lung cancer who have progressed after chemoimmunotherapy [3]. Another trial is investigating ivosidenib plus mFOLFOXIRI and celecoxib for BRAF V600E-mutant colorectal cancer that is refractory to BRAF-targeted therapy [4]. These trials are ongoing; their results do not yet establish efficacy for any indication.

If you are reading this for personal health reasons

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

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