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Impact of nitric oxide's bidirectional role on glaucoma: focus on Helicobacter pylori –related nitrosative stress
Author(s) -
Papaefthymiou Apostolis,
Doulberis Michael,
Katsinelos Panagiotis,
Liatsos Christos,
Polyzos Stergios A.,
Kotronis Georgios,
Papanikolaou Katerina,
Kountouras Jannis
Publication year - 2020
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.14253
Subject(s) - nitric oxide , glaucoma , peroxynitrite , intraocular pressure , pathophysiology , homeostasis , endogeny , helicobacter pylori , overproduction , inflammation , immunology , medicine , chemistry , microbiology and biotechnology , biology , ophthalmology , pathology , biochemistry , enzyme , superoxide
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.