Target intelligence / Profile preview

Angiogenesis promotion via paracrine signaling factors

Molecular classification
Other (biological process), Growth factors (VEGF, FGF, PDGF, TGF-β, Angiopoietin), Cytokines (e.g., IL-6, IL-8, TNF-α), Chemokines (e.g., CXCL8), Peptides, Extracellular vesicles as carriers
01

Overview

The phrase "angiogenesis promotion via paracrine signaling factors" encompasses the complex, localized secretion of growth factors, cytokines, and chemokines by cells to stimulate the formation of new blood vessels in neighboring tissues. Paracrine signaling is a key mechanism by which endothelial and stromal cells coordinate angiogenesis during normal development, tissue repair after injury, and pathological states such as tumor growth. The most prominent growth factors mediating this effect are vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and others, which bind their respective transmembrane receptors on endothelial cells to activate signal transduction cascades that promote cell proliferation, migration, survival, and differentiation[1][7][8]. Inhibiting these pathways forms the basis for many anti-angiogenesis drugs used clinically, especially in cancer therapy, but can lead to significant safety concerns due to VEGF’s role in maintaining normal vasculature[4][7].

Other names
Angiogenesis via paracrine factorsParacrine angiogenic factors signalingParacrine-mediated angiogenesis
02

Mechanism of action

Inhibition of growth factor binding to receptor (e.g., anti-VEGF antibody); Blockade of receptor tyrosine kinase activation (small-molecule kinase inhibitors); Disruption of ligand-induced signal transduction for angiogenesis

03

Biological functions

Cell–cell communicationPromotion of angiogenesis (blood vessel formation)Regulation of endothelial cell proliferation, migration, survival, and tube formationResponse to tissue injury (wound healing, regeneration)Modulation of immune responses
04

Disease associations

Cancer (tumor angiogenesis and metastasis)Cardiovascular disease (ischemia, tissue repair)Wound healing (tissue regeneration)Inflammatory conditionsOther (organ development, tissue engineering)
05

Safety considerations

Impaired wound healingHypertensionThromboembolic eventsHemorrhageProteinuriaGastrointestinal perforationCardiovascular complications
06

Interacting drugs

Anti-VEGF drugs: Bevacizumab, aflibercept, ranibizumab

2 more in the full profile.

07

Biomarkers

Circulating VEGF levelsSoluble VEGF receptorExpression of angiogenic factors in tumor or tissue biopsies (VEGF, FGF, PDGF)Endothelial markers (CD31, von Willebrand factor)

Beyond the preview

Go deeper on Angiogenesis promotion via paracrine signaling factors.

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Angiogenesis promotion via paracrine signaling factors.

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call