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Hedi Raizer

Journal 6 min read

Which peptides are studied in relation to angiogenesis?

A research-supply overview of peptides and related agents studied in angiogenesis models, spanning cathelicidin LL-37, platelet-released growth factors, adipokines, and metabolic or antibody-based modulators.

peptides-pro Editorial

Angiogenesis research draws on several distinct molecular classes, and the peptides studied in this context are not a single family. They include host-defence cathelicidins such as LL-37, a 37-residue antimicrobial peptide; platelet-derived growth factor mixtures released from platelet lysates; adipose-tissue-secreted adipokines; and small-molecule or antibody agents that intersect angiogenic signalling indirectly. The evidence block for this page does not supply a sequence, molecular formula, or molecular weight for any of these compounds, so no such identifiers are stated here.

The pathway most consistently named across the assembled evidence is the vascular endothelial growth factor (VEGF) axis and its receptor family, with NF-κB/IL-6 signalling, the PI3K-Akt-mTOR cascade, and thymidine phosphorylase-linked metabolic flux appearing as additional mechanistic nodes in specific models [3][7][8][9].

Research Studies

Cathelicidin LL-37 and angiogenesis inhibition in gastric cancer

Cathelicidin LL-37, an antimicrobial peptide with context-dependent activity in cancer, was examined in gastric cancer models. The reported finding is that LL-37 inhibits angiogenesis and migration in gastric cancer via inhibition of NF-κB/IL-6 signalling [9]. This places the peptide on the anti-angiogenic side of the ledger in that tumour context, in contrast to the pro-angiogenic roles reported for other peptide classes below.

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 with translational potential for tissue repair. In what the authors present as the first in vitro study of its kind, PRGF exerted pro-angiogenic effects at a working concentration of 10% in an endothelial cell-based model. The model integrated targeted gene expression analysis, array-based profiling of angiogenesis-related proteins, and functional endothelial tube formation assays [5]. These are in vitro findings; no animal or human outcome data are reported in the evidence block for PRGF.

Nicotinamide mononucleotide and choroidal neovascularization in mice

Nicotinamide mononucleotide (NMN) was evaluated for its capacity to modulate the neurovascular inflammatory microenvironment and blunt tissue remodelling in neovascular age-related macular degeneration. A laser-induced choroidal neovascularization (CNV) model was established in C57BL/6J mice, with CNV lesion size quantified on RPE/choroid flat mounts. Immunostaining assessed myeloid cell accumulation and fibrosis-associated remodelling, while 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 [6]. The reported outcome is attenuation of inflammatory activation, choroidal neovascularization, and lesion-associated remodelling. This is animal and in vitro evidence.

Adipokines and angiogenic mechanisms in preeclampsia

Adipokines are bioactive peptides secreted by adipose tissue. A review of preeclampsia — a multifactorial hypertensive disorder of pregnancy — summarizes findings from multiple studies indicating that adipokines may contribute to pathogenesis through mechanisms involving inflammation, angiogenesis, and endothelial dysfunction [10]. This is a review-level synthesis rather than a primary experimental result.

Preeclamptic placental macrophages and impaired angiogenesis in vitro

In preeclampsia, aberrant macrophage polarization has been implicated in disease. Endothelial cells exposed to preeclamptic placental macrophages showed increased oxidative stress and impaired angiogenesis in vitro [12]. This is an in vitro endothelial model; the direction of the effect on angiogenesis is impairment rather than promotion.

2-deoxy-D-ribose and thymidine phosphorylase-linked angiogenic signalling

2-deoxy-D-ribose (2dDR) is a metabolite rather than a peptide, but it appears in the angiogenesis literature through its relationship with thymidine phosphorylase (TP). Oncogenic drivers can elevate 2dDR levels by directing carbon flux toward the pentose phosphate pathway and nucleotide biosynthesis, increasing substrate availability for nucleoside phosphorylases, with TP as the primary enzymatic source of 2dDR [8]. TP is itself an established angiogenic enzyme, which is why this metabolic node is studied alongside peptide and protein modulators.

Insulin resistance, monoclonal antibodies, and angiogenic signalling

Insulin resistance contributes to hyperinsulinaemia, disruption of insulin-like growth factor signalling, chronic inflammation, and metabolic remodelling, fostering 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. The review proposes that IGF-1R, IL-6, IL-1β, TNF-α, PD-1, PD-L1, and CTLA-4 monoclonal antibodies could be beneficial by inhibiting inflammatory signalling [7]. This is a review-level mechanistic synthesis, not a primary trial result.

Ivonescimab, a bispecific PD-1/VEGF antibody, in advanced NSCLC

Ivonescimab is a bispecific PD-1/VEGF antibody. A Phase II clinical trial is investigating the efficacy of combining gemcitabine, a chemotherapy agent, with ivonescimab in patients with advanced non-small cell lung cancer who have experienced disease progression following chemoimmunotherapy. 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, potentially enhancing antitumour activity [3]. This is a registered trial record; results are not reported 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 [2]. Several of these secreted factors are peptides or small proteins, and matrix remodelling is mechanistically adjacent to the angiogenic programmes described above. This is a review.

Zinc silicate microspheres and wound microenvironment remodelling

Zinc silicate flower-like microspheres (ZnSi FMPs) were designed with a controlled hierarchical architecture to achieve chronic wound repair by mediating bacterial metabolic interference and microenvironment remodelling. The nanosheet structure with sustained Zn2+ release endows the material with pH-independent antibacterial activity [1]. This is an inorganic material rather than a peptide, but it is included here because wound repair endpoints overlap with the angiogenic endpoints studied for PRGF and related agents.

Comparison of evidence contexts

AgentClassModel / populationReported angiogenesis-related finding
Cathelicidin LL-37Antimicrobial peptideGastric cancerInhibits angiogenesis and migration via NF-κB/IL-6 inhibition [9]
PRGFPlatelet lysate (cell- and fibrin-free)Endothelial cells in vitroPro-angiogenic effects at 10% working concentration [5]
NMNNicotinamide nucleotideC57BL/6J mouse laser-induced CNV; bEnd.3 cells in vitroAttenuates inflammatory activation, CNV, and lesion-associated remodelling [6]
AdipokinesAdipose-secreted peptidesPreeclampsia (review)Implicated in inflammation, angiogenesis, and endothelial dysfunction [10]
Preeclamptic placental macrophage exposureCell-conditioned in vitro systemEndothelial cells in vitroIncreased oxidative stress and impaired angiogenesis [12]
IvonescimabBispecific PD-1/VEGF antibodyAdvanced NSCLC, post-chemoimmunotherapy (Phase II)Targets PD-1 and VEGF pathways [3]

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