While low concentrations of HS have been found to activate FGF2 by facilitating growth factor ligand–receptor complex formation [27], high concentrations of HS compete to bind both the ligand and receptor, preventing the complex formation and inhibiting downstream signaling [28]; thereby, counteracting severe shedding of HS in sepsis with exogenous HS may potentially inhibit rather than activate endothelial reparative pathways. Here, FGF2 is linked to Sepsis.