langiogenesi

Langiogenesi, or lymphangiogenesis, is the growth of lymphatic vessels from pre-existing lymphatic endothelium. It is a key process in embryonic development, tissue remodeling, and disease, enabling the expansion and remodeling of the lymphatic vasculature. Langiogenesi is distinct from angiogenesis, which involves blood vessels, though the two processes share signaling cues and can interact in tissues.

The process is driven by lymphatic endothelial cells (LECs) that express markers such as PROX1, LYVE-1, and podoplanin, and by signaling through VEGF-C and VEGF-D binding to VEGFR-3. Activation leads to LEC proliferation, migration, and sprouting; transcription factors like PROX1 and FOXC2 specify lymphatic identity and valve formation. Macrophages and tumor cells may provide VEGF-C/D; MMPs remodel the extracellular matrix to permit sprouting.

In development, PROX1 guides venous endothelial cells toward a lymphatic fate, establishing a network that maintains tissue fluid balance and enables immune cell trafficking to lymph nodes. Lymphatics also facilitate intestinal lipid absorption via lacteals. Langiogenesi persists in adulthood during wound healing and tissue repair, adapting lymphatic networks to local needs.

Pathologically, excessive or insufficient lymphangiogenesis contributes to cancer metastasis, chronic inflammation, and lymphedema. Therapies aim to modulate lymphangiogenesis: inhibiting VEGFR-3 signaling to limit tumor spread, or promoting VEGF-C–driven growth to enhance drainage in lymphedema or tissue repair. Research explores gene therapy, protein traps, and antibodies as means to tune lymphatic vessel growth.

Assessment relies on lymphatic markers (PROX1, LYVE-1, podoplanin) and VEGFR-3 expression, with imaging advances enabling lymphatic-specific visualization. Model organisms such as mice and zebrafish illuminate the genetic control of lymphangiogenesis and its interactions with the blood vasculature and immune system.