The Lamina Cribrosa (LC) is a thin disc located at the head of the optic nerve. It not only provides a support structure within the optic nerve head, serving as a framework for gathering axons, but it is also crucial for blood supply and drainage. The LC has addi- tional roles in stabilizing the pressure difference between the intra-ocular pressure (IOP) in the vitreous chamber, and the retrolaminar tissue pressure (RLTp). Elevated IOP poses a significant risk for optic nerve damage, leading to a progressive vision impairment and blindness, as observed in glaucoma. The proposed model aims to integrate mechanical and hemodynamic perspectives. Our starting point was to set an analogy with the prototypical models of species intercalation within an elastic lattice: after having transformed quantities appropriate to a diffusing species into corresponding quantities suitable for a saturated porous material, the re- sulting power balance laws, for forces and fluid filling the porosity network, lead to a constitutive characterization coupling deformation and stresses with porosity, ultimately yielding Darcy’s law. This characterization relies on the expression of the free energy, particularly its dependence on porosity: a non monotonic profile of the porosity field while increasing the state of stress of the solid matrix naturally emerges as an effect of the cou- pled dynamics, determining a stiffening of the solid matrix subject to high hydrostatic pressure: this aspect differentiates our model with respect to the standard poroelastic ones. Subsequently, we highlight the clinical relevance of the model in describing the changes LC undergoes when it is subject to a relevant increasing of IOP: through nu- merical simulations, we illustrate how an elevated IOP leads to high shear deformations at the periphery of the lamina, greatly impacting both on porosity (with the emergence of drained regions) and blood perfusion. We emphasize as the stiffening effect on the solid matrix is a crucial feature to describe the the non-monotonic behavior of the blood perfusion under high IOP, as clinically observed in in-vivo.