Primary open-angle glaucoma (POAG) is a leading cause of irreversible and preventable blindness and ocular hypertension is the strongest known risk factor. With current classes of drugs, management of the disease focuses on lowering intraocular pressure (IOP). Despite of their use to modify the course of the disease, none of the current medications for POAG is able to reduce the IOP by more than 25%–30%. Also, some glaucoma patients show disease progression despite of the therapeutics. This paper examines the new described physiological targets for reducing the IOP. The main cause of elevated IOP in POAG is thought to be an increased outflow resistance via the pressure-dependent trabecular outflow system, so there is a crescent interest in increasing trabecular meshwork outflow by extracellular matrix remodeling and/or by modulation of contractility/TM cytoskeleton disruption. Modulation of new agents that act mainly on trabecular meshwork outflow may be the future hypotensive treatment for glaucoma patients. There are also other agents in which modulation may decrease aqueous humour production or increase uveoscleral outflow by different mechanisms from those drugs available for glaucoma treatment. Recently, a role for the ghrelin-GHSR system in the pathophysiology modulation of the anterior segment, particularly regarding glaucoma, has been proposed.

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Background: The inflammatory hypothesis of depression implies that an unbalance of the immune system may trigger abnormal responses, affecting neural signalling mediators and the hypothalamic-pituitary-adrenal axis. This theory underlies a bidirectional hypothesis on the influence of depressive symptoms in the clinical course of chronic inflammatory disorders (CID), as well as in the genesis of mood disturbances. We aim to review current knowledge on depressive disorders and chronic inflammatory diseases as comorbidities and the underlying pathophysiologic mechanisms.

Purpose The purpose of this work is to investigate the effect of ghrelin in a primate choroid retinal cell line cultured under hyperglycemic conditions and its effect on the early changes of diabetic retinopathy in an animal model of type1 diabetes mellitus (DM1). Methods A RF/6a cell line was used in the in vitro assay. Cell migration was assessed using the wound healing assay under increasing (0‐300mM) glucose concentrations. To test its effect, ghrelin was added (10‐5‐10‐10nM) to the cell cultures for 24h. Positive controls had VEGF added to the medium. For the in vivo studies, diabetic Wistar rats received intravitreal injections of either ghrelin (81nM) or saline every 4 weeks for 3 months. Vascular permeability was assessed using the Evans blue assay. Results Increasing concentrations of glucose show a reduction in cell migration distance. We defined 10 mM of glucose as the basal and 250 mM as the hyperglycemic condition. At a concentration of 10‐8 nM ghrelin potentiates the reduction of migration induced by the hyperglycemic medium, and reduces the migration induced by VEGF. Regarding the in vivo model, diabetic animals treated with intravitreal ghrelin injections showed no alteration in vascular permeability, when compared with diabetic controls. Conclusion Ghrelin reduces cell migration in choroid‐retinal cells under hyperglycemic media, but appears to have no effect on the vascular permeability in a DM1 animal model.