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Review ArticleOpen Access

A Review of Metabolic Sensors in Glaucoma Volume 3 - Issue 1

Powell S MB1, Irnaten M1 and O Brien CJ MD1,2*

  • 1Department of Ophthalmology, Mater Misericordiae University Hospital, Ireland
  • 2School of Medicine and Medical Science, University College Dublin, Ireland

Received:November 07, 2020;   Published:November 13, 2020

Corresponding author: Colm O’Brien, Institute of Ophthalmology, School of Medicine and Medical Science, University College Dublin, Dublin, Ireland

DOI: 10.32474/TOOAJ.2020.03.000155

 

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Abstract

Glaucoma is the second leading cause of irreversible blindness worldwide. It is a multifactorial, progressive, chronic optic neuropathy that is characterized by loss of retinal ganglion cells (RGC) and optic nerve head (ONH) cupping including extra cellular matrix (ECM) remodelling and fibrosis at the lamina cribrosa (LC). Clinically this results in chronic, progressive peripheral visual field loss. The pathogenesis of glaucoma is not yet fully understood. Therefore, there is an urgent need to identify and target the underlying mechanisms governing ECM remodelling of the LC, in order to stop the progressive, chronic damage to the LC/ONH and irreversible visual field loss. This review identifies and examines some of the key metabolic processes and cellular sensors involved in the pathogenesis of ECM fibrosis in general but herein specifically in glaucoma, including mitochondrial dysfunction and adenosine monophosphate activated protein kinase (AMPK) upregulation. Furthermore, the development of novel therapeutics such as nicotinamide (NAM) and metformin are discussed as promising potential future therapeutic options for glaucoma.

Keywords: Glaucoma; Fibrosis; Extracellular Matrix (Ecm) Mitochondrial Dysfunction; Adenosine Monophosphate Activated Protein Kinase (Ampk); Nicotinamide (Nam); Metformin

Abstract| Introduction| Fibrosis| Mitochondrial Dysfunction in Glaucoma| The Role of Nicotinamide (NAM) in Glaucoma| AMPK as a Sensor of Cellular Stress| Future Directions and Conclusion| Conflict of Interest| References|