Silva Sosa, A.; Dejda, A.; Gaelle stephanie, M.; Cagnone, G.; kawtar, z.; Diaz, R.; Guber, V.; Mallette, F. A.; Joyal, J.-S.; Sapieha, P.; OUBAHA, M.

The mammalian eye develops in concert with coordinated growth and remodeling of three vascular networks: the transient hyaloid vasculature, the choroid and retinal plexus. While retinal and choroidal systems support visual function in the mature eye, the hyaloid network plays a vital yet temporary role supporting the developing lens and inner retina. Postnatal regression of the hyaloid network is essential for optical clarity, yet the mechanisms guiding the process remain incompletely understood. Using single-cell RNA sequencing, we show that postnatal mouse hyaloid cells are broadly senescent. Hyaloid vascular smooth muscle, endothelial and immune cells display cell-cycle arrest together with a distinctive secretory programme marked by Cdkn1a and expression of SASP factors. Genetic ablation of Cdkn1a impedes normal hyaloid regression, demonstrating that developmental senescence is essential for timely vascular remodeling and functions alongside apoptosis and macrophage-mediated clearance. These findings identify a previously unrecognized senescence-driven mechanism orchestrating hyaloid vessel involution during early ocular development, broadening the understanding of vascular remodeling in the eye.