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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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Related Experiment Video

Updated: May 2, 2026

Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting
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Inflammation-associated lymphangiogenesis: a double-edged sword?

Honsoul Kim, Raghu P Kataru, Gou Young Koh

    The Journal of Clinical Investigation
    |March 5, 2014
    PubMed
    Summary

    Inflammation-associated lymphangiogenesis (IAL) actively contributes to inflammatory disorders. Therapies targeting key signaling pathways like VEGF-C/VEGFR-3 show promise in preclinical and clinical studies.

    Area of Science:

    • Lymphatic biology
    • Inflammation research
    • Vascular biology

    Background:

    • Lymphangiogenesis and lymphatic vessel remodeling are key processes in inflammation.
    • Inflammation-associated lymphangiogenesis (IAL) plays an active role in inflammatory disease pathophysiology.
    • VEGF-C/VEGFR-3 and VEGF-A/VEGF-R2 pathways are critical regulators of IAL.

    Purpose of the Study:

    • To review recent advances in lymphatic biology related to inflammatory conditions.
    • To summarize preclinical and clinical therapies that modulate IAL.
    • To highlight the role of IAL in inflammatory disorders.

    Main Methods:

    • Literature review of recent achievements in lymphatic biology.
    • Summary of preclinical and clinical studies on IAL modulation.

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  • Focus on VEGF-C/VEGFR-3 and VEGF-A/VEGF-R2 signaling pathways.

    • Main Results:

    • IAL is an active participant in inflammatory conditions, not just a passive outcome.
    • Targeting VEGF-C/VEGFR-3 and VEGF-A/VEGF-R2 pathways offers therapeutic potential.
    • Prolymphangiogenic and antilymphatic treatments have shown benefits in studies.

    Conclusions:

    • Understanding IAL is crucial for developing new treatments for inflammatory diseases.
    • Targeted therapies modulating lymphatic vessel dynamics hold promise for managing inflammation.
    • Recent research provides a strong foundation for clinical applications in IAL.