Impaired Angiogenesis in Diabetic Wounds (2D)
Interactive 2D reaction-diffusion simulator: a VEGF field diffuses from hypoxic wound tissue while an endothelial-density field spreads from the capillary margin by diffusion, volume-limited chemotaxis up the VEGF gradient, and logistic proliferation -- throttled by the same glucose-driven HIF-1alpha suppression as the 3D tip-cell model.
This is the same VEGF-chemotaxis biology as the 3D tip-cell simulator, recomputed as two coupled reaction-diffusion fields on a grid instead of discrete sprouting agents: a VEGF concentration that diffuses out of hypoxic wound tissue, and an endothelial-cell density that diffuses, proliferates and climbs that VEGF gradient by volume-limited chemotaxis. Chronic hyperglycemia is modeled the same way it is in the 3D version — by suppressing HIF-1α stabilization, which throttles both the VEGF source and the endothelial field's chemotactic gain — so raising the glucose slider visibly starves the advancing front before it reaches the wound bed, and PHD-inhibitor therapy rescues it.
2D reaction-diffusion simulator of diabetic wound angiogenesis: a VEGF concentration field diffuses out of hypoxic wound tissue while an endothelial-cell density field spreads from the capillary margin by diffusion, volume-limited chemotaxis up the VEGF gradient, and logistic proliferation, all gated by the same glucose-driven HIF-1alpha suppression as the 3D tip-cell model.
2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install