Impact of nitric oxide's bidirectional role on glaucoma: focus on Helicobacter pylori–related nitrosative stress. Issue 1 (23rd October 2019)

• Record Type: Journal Article
• Authors: Papaefthymiou, Apostolis; Doulberis, Michael; Katsinelos, Panagiotis; Liatsos, Christos; Polyzos, Stergios A.; Kotronis, Georgios; Papanikolaou, Katerina; Kountouras, Jannis
• Is Part Of: Annals of the New York Academy of Sciences. Volume 1465:Issue 1(2020)
• Page Start: 10
• Page End: 28
• Publication Date: 2019-10-23
• Subjects: nitric oxide -- NO -- Helicobacter pylori -- Hp -- glaucoma; Medical sciences -- Periodicals; Medicine -- Periodicals; Science -- Periodicals; 610
• DOI: 10.1111/nyas.14253
• Languages: English
• ISSNs: 0077-8923

Abstract

Abstract: Nitric oxide (NO), a small molecule generated ubiquitously, targets a plethora of tissues to regulate both physiological and pathophysiological functions. NO overproduction, stimulated by microenvironmental conditions, is the main component that dysregulates the tight balance between its beneficial and damaging roles in ocular homeostasis. Considering the protective functions of NO against glaucoma, its endogenous release facilitates aqueous humor drainage and regulates ocular blood flow, maintaining a normal intraocular pressure. NO overproduction generates free radicals, such as peroxynitrite, which induce a vicious circle of vascular disharmony and dysregulation, transient ischemia, nitrosative stress, neuronal degeneration, and permanent glaucomatic injury. Helicobacter pylori ( Hp ) is considered a burdening factor of glaucoma. NO overproduction and possible systematic dispersion in Hp infection ( Hp ‐I) could suggest a potential pathophysiological bridge between these conditions. In this review, we aim to elucidate the role of NO in glaucoma with respect to Hp ‐I, with the aim to stimulate further studies. Abstract : In this review, our studies reported a strong correlation between aqueous humor (AH) and serum‐specific anti‐ Hp IgG levels in patients with glaucoma. Therefore, we hypothesized that anti‐ Hp antibodies may circulate in the bloodstream and enter the aqueous circulation via the blood–AH barrier.