Molecular changes in glaucomatous trabecular meshwork. Correlations with retinal ganglion cell death and novel strategies for neuroprotection

Sergio C. Saccà, Stefania Vernazza, Eugenio Luigi Iorio, Sara Tirendi, Anna Maria Bassi, Stefano Gandolfi, Alberto Izzotti

Research output: Chapter in Book/Report/Conference proceedingChapter


Glaucoma is a chronic neurodegenerative disease characterized by retinal ganglion cell loss. Although significant advances in ophthalmologic knowledge and practice have been made, some glaucoma mechanisms are not yet understood, therefore, up to now there is no effective treatment able to ensure healing. Indeed, either pharmacological or surgical approaches to this disease aim in lowering intraocular pressure, which is considered the only modifiable risk factor. However, it is well known that several factors and metabolites are equally (if not more) involved in glaucoma. Oxidative stress, for instance, plays a pivotal role in both glaucoma onset and progression because it is responsible for the trabecular meshwork cell damage and, consequently, for intraocular pressure increase as well as for glaucomatous damage cascade. This review at first shows accurately the molecular-derived dysfunctions in antioxidant system and in mitochondria homeostasis which due to both oxidative stress and aging, lead to a chronic inflammation state, the trabecular meshwork damage as well as the glaucoma neurodegeneration. Therefore, the main molecular events triggered by oxidative stress up to the proapoptotic signals that promote the ganglion cell death have been highlighted. The second part of this review, instead, describes some of neuroprotective agents such as polyphenols or polyunsaturated fatty acids as possible therapeutic source against the propagation of glaucomatous damage.

Original languageEnglish
Title of host publicationProgress in Brain Research
EditorsGiacinto Bagetta, Carlo Nucci
PublisherElsevier B.V.
Number of pages38
ISBN (Print)9780128211069
Publication statusPublished - 2020

Publication series

NameProgress in Brain Research
ISSN (Print)0079-6123
ISSN (Electronic)1875-7855


  • Aqueous humor proteome
  • Endothelial dysfunction
  • Extracellular matrix
  • Glaucoma pathogenesis
  • Neuroprotection
  • Omega-3
  • Polyphenols
  • Schlemm's canal
  • Trabecular meshwork

ASJC Scopus subject areas

  • Neuroscience(all)


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