Journal
EXPERIMENTAL EYE RESEARCH
Volume 183, Issue -, Pages 88-97Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exer.2018.11.005
Keywords
Glaucoma; Risk factors; Biomechanics; Ischemia; Astrocytes; Glia; Microglia; Oxidative stress; Metabolic stress; Mitochondria; Neurotrophic factors
Categories
Funding
- Canadian Institutes of Health Research
- Natural Sciences and Engineering Research Council of Canada
- Glaucoma Research Society of Canada
- Western Hospital Glaucoma Research Chair
- Vision Science Research Program (VSRP) Fellowship
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Glaucoma describes a distinct optic neuropathy with complex etiology and a variety of associated risk factors, but with similar pathological endpoints. Risk factors such as age, increased intraocular pressure (IOP), low mean arterial pressure, and autoimmune disease, can all be associated with death of retinal ganglion cells (RGCs) and optic nerve head remodeling. Today, IOP management remains the standard of care, even though IOP elevation is not pathognomonic of glaucoma, and patients can continue to lose vision despite effective IOP control. A contemporary view of glaucoma as a complex, neurodegenerative disease has developed, along with the recognition of a need for new disease modifying retinal treatment strategies and improved outcomes. However, the distinction between risk factors triggering the disease process and retinal injury responses is not always clear. In this review, we attempt to distinguish between the various triggers, and their association with subsequent key RGC injury mechanisms. We propose that distinct glaucomatous risk factors result in similar retinal and optic nerve injury cascades, including oxidative and metabolic stress, glial reactivity, and altered inflammatory responses, which induce common molecular signals to induce RGC apoptosis. This organization forms a coherent disease framework and presents conserved targets for therapeutic intervention that are not limited to specific risk factors.
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