Angiogenesis
Angiogenesis is the biological process through which new blood vessels form from pre-existing vasculature.
Angiogenesis is the biological process through which new blood vessels form from pre-existing vasculature. It is regulated by coordinated endothelial-cell activation, proliferation, migration, extracellular-matrix remodeling, and maturation of vascular structures. Vascular endothelial growth factor (VEGF) is a major pro-angiogenic signal, while tissue oxygenation, inflammation, reactive oxygen species, macrophage activity, and pathways such as HIF-1α influence the balance between vascular growth and regression.
Physiological angiogenesis contributes to wound healing, tissue regeneration, and tissue remodeling, including vascular repair after ischemic injury. In pathological settings, excessive or disorganized angiogenesis can support tumor growth and progression, whereas inadequate angiogenesis may limit repair in ischemic or injured tissues. Consequently, angiogenesis is both a therapeutic objective—when vascularization is desired—and a treatment target, particularly in cancer. Experimental studies commonly assess angiogenesis through endothelial-cell migration and proliferation, vascular markers such as CD31, and the formation of vascular structures in biomaterials or tissue models.
Rebuilt from PubMed 18 Sept 2026 · no new papers today
Where the papers sit
10 papers study angiogenesis directly. The themes below are drawn from those 10.
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Growth Factor Angiogenesis and Repair : Controlled delivery and pathway targeting are moving angiogenic repair beyond single-factor treatment. VEGF, FGF-2, PDGF, HIF-1α and the ERβ–ANGPT2 axis recur in cardiac, cerebral and placental vascular remodeling. 4 papers · 40%
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Cytotoxicity and Angiogenic Control : Apoptosis, G2/M arrest and reduced migration recur across bioactive therapeutic studies. ROS generation, tubulin inhibition and exosome signaling link breast-cancer treatment with oral-ulcer repair. 3 papers · 30%
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Immune–Angiogenesis Cancer Therapy : Antiangiogenic drugs are increasingly paired with immune modulation rather than used alone. Lenvatinib, sunitinib, PD-L1 inhibition, vascular normalization, immune monitoring and biomarkers recur across liver, renal and lung cancer settings. 3 papers · 30%
Recent Findings on angiogenesis
Growth Factor Vascular Remodeling: Shoutai Wan and Danshen-Chuanxiong promote angiogenesis through defined signaling pathways involving ERβ–ANGPT2 and CPT1/HIF-1α, respectively 42726298Sep42431282Jul. Supramolecular hydrogels and affibody-conjugated hydrogels coordinate vascular endothelial growth factor, fibroblast growth factor-2, and platelet derived growth factor delivery for myocardial repair or vascular network formation 42492872Jul42447931Jul. Sequential vascular endothelial growth factor, fibroblast growth factor-2, and platelet derived growth factor delivery produced greater network length and branching than untreated microvascular fragments, although perivascular coverage remained similar across treatment groups 42447931Jul. The findings support pathway-directed vascular repair that combines controlled growth factor presentation with vascular maturation and tissue protection. Future work is moving toward temporally coordinated delivery and more precise regulation of vascular remodeling.
Immunoangiogenic Cancer Therapy: Lenvatinib and sunitinib pair angiogenesis inhibition with immune modulation to improve tumor control and immunogenicity 42708433Sep42262196Jun42392517Jul. Lenvatinib with PD-L1 inhibition increased CD8+ T cells, reduced Tregs, and shifted cytokines toward increased IFN-γ and TNF-α in liver transplant recipients with hepatocellular carcinoma 42262196Jun. A pH-responsive GelMA hydrogel combined sunitinib with copper oxide nanoparticles, using cuproptosis, reactive oxygen species generation, damage-associated molecular patterns, and macrophage reprogramming to suppress clear cell renal cell carcinoma 42392517Jul. Translation remains dependent on molecular heterogeneity, variable timing of vascular normalization and immune activation, and biomarker-driven immune monitoring rather than PD-L1 expression alone 42708433Sep.
Combretastatin A4-chalcone hybrids and menstrual blood stem cell-derived exosomes suppress cancer-cell survival, migration, and angiogenic signaling through overlapping cytotoxic mechanisms 42647402Aug42159846May. The hybrids caused tubulin polymerization inhibition, G2/M phase cell cycle arrest, and apoptosis, while exosomes increased reactive oxygen species, altered BAX and BCL-2, and downregulated VEGF and MMP-2 42647402Aug42159846May. PAT nanoparticles produced a different therapeutic profile by scavenging free radicals, limiting M1 macrophage polarization, promoting M2 polarization, and enhancing migration and angiogenesis during oral ulcer healing 41989033Apr. Together, these findings direct angiogenesis toward either inhibition in cancer models or promotion in tissue repair, with nanoparticle design and biologic cargo shaping the therapeutic outcome.
Written from 10 PubMed abstracts, each one cited by PMID above. Published: 2026-09-10. Last written: 2026-09-13 by GPT. Drafted by language models from published abstracts; not medical advice.