Glaucome : un traitement qui permet de voir plus loin

Primary open-angle glaucoma affects about 70 million people and is predicted to account for over 11 million cases of blindness by 2020 [1], [2]. Its prevalence continues to increase as the population ages. Glaucoma is a retinal neuropathy characterized by retinal ganglion cell death. Pathological elevation of intraocular pressure (IOP), namely ocular hypertension (OHT), is the most critical risk factor for both the development and the progression of the disease [3]. OHT is often diagnosed several years before detecting the neuropathy. It is attributed to a decrease in trabecular meshwork (TM) outflow facility to aqueous humor (AH) caused by tissue degeneration whose primary mechanisms are still unclear. Classical antiglaucoma treatments reduce the abnormally elevated IOP but do not target directly the initial TM pathology. In clinical practice, progressive therapeutic inefficiency in controlling both the elevation of IOP and neuropathy often occurs [4]. The lack of specific therapies for the TM pathology, which is still developing in well-treated patients, could be responsible for progressive treatment inefficiency coupled with neuropathy worsening and sometimes blindness. TM degeneration has largely been demonstrated as the main cause of aqueous outflow resistance leading to OHT in primary open-angle glaucoma (5]. The main glaucoma-related trabecular modifications resemble age-related TM degeneration and involve accumulation of trabecular extracellular matrix together with a decrease in TM cellularity as previously described by our group and others [6]–[9]. Trabecular cell (TC) loss that occurs in glaucoma is known to develop through apoptotic phenomena and was found as a characteristic of primary open-angle glaucoma [10], but its causal mechanisms are still unknown. Stromal cell-derived factor-1 (SDF-1), termed CXCL12, belongs to the CXC subfamily

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