0
0This article demonstrates that VEGFR2 is an essential collaborator in the sprouting of lymphatic vessels, a process previously thought to be driven primarily by VEGFR3. Through genetic experiments in mice, researchers found that while VEGFR2 cannot trigger vessel growth on its own, its absence prevents lymphatic cells from forming new branches. The study explains that VEGF-C coordinates these two receptors to balance cell multiplication with organized vessel expansion. This discovery highlights that PI3Kα signaling regulates how these receptors appear on the cell surface to ensure functional vascular networks. Ultimately, the findings suggest that current anti-angiogenic therapies targeting VEGFR2 could be repurposed to treat diseases involving abnormal lymphatic growth.
References:
Schoofs H, Zhang Y, Ortsäter H, et al. VEGFR2 is required for VEGF-C–VEGFR3–PI3Kα-mediated sprouting lymphangiogenesis[J]. Nature Communications, 2026, 17(1): 4380.
