Abstract
Aims: To assess the levels of hepcidin prohormone (Hep) in aqueous humor and plasma of human eyes with primary open-angle glaucoma (POAG) and to correlate their concentrations with the severity of glaucoma. Methods: Sixty patients with POAG and forty five patients with senile cataract (control group) were enrolled in the study prospectively. Aqueous humor samples were obtained by paracentesis from glaucoma and cataract patients who were undergoing elective surgery. Aqueous humor and corresponding plasma samples were analyzed for Hep concentrations by enzyme-linked immunosorbent assay. Results: Hep levels were significantly lower in aqueous humor of POAG patients with respect to the comparative group of cataract patients (P
Highlights
Glaucoma, which is characterized by retinal ganglion cell (RGC) apoptosis, is the prominent cause of blindness
RGC apoptosis may be the result of increased intraocular pressure, neurotoxicity and apoptosis [1], extracellular matrix (ECM) changes [2], oxidative stress [3], and hypoxia due to ocular and systemic vascular dysregulation [4]
The control group consisted of 45 non-pathological cataract patients, whose age ranged from 53 to 75 years were scheduled for cataract surgery
Summary
Glaucoma, which is characterized by retinal ganglion cell (RGC) apoptosis, is the prominent cause of blindness. Hepcidin prohormone (Hep) is a small peptide produced in the liver. Human Hep is produced from an 84 amino acid precursor, including a putative single peptide. Hep is an important peptide hormone that plays a critical role in the regulation of iron efflux from numerous cell types, including intestinal cells, macrophages, and hepa-. Hep binds to and induces the degradation of ferroportin, an iron exporter expressed in specific cell types, as the receptor for this iorn-regulatory hormone. [5] The binding of hepcidin to ferroportin lesds internalization of the iron exporter with subsequent degradation in lysosomes Hep binds to and induces the degradation of ferroportin, an iron exporter expressed in specific cell types, as the receptor for this iorn-regulatory hormone. [5] The binding of hepcidin to ferroportin lesds internalization of the iron exporter with subsequent degradation in lysosomes
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