Year: 2014
Type: review
Abstract: There is growing evidence that chronic inflammation plays a role in both the development and progression of diabetic retinopathy. There is also evidence that molecules produced as a result of hyperglycemia can activate microglia. However the exact contribution of microglia, the resident immune cells of the central nervous system, to retinal tissue damage during diabetes remains unclear. Current data suggest that dysregulated microglial responses are linked to their deleterious effects in several neurological diseases associated with chronic inflammation. As inflammatory cytokines and hyperglycemia disseminate through the diabetic retina, microglia can change to an activated state, increase in number, translocate through the retina, and themselves become the producers of inflammatory and apoptotic molecules or alternatively exert anti-inflammatory effects. In addition, microglial genetic variations may account for some of the individual differences commonly seen in patient's susceptibility to diabetic retinopathy.
Source: Journal of Ophthalmology
DOI: 10.1155/2014/705783
Authors: Jeffery G. Grigsby, Sandra M. Cardona, Cindy E. Pouw, Alberto Muniz, Andrew S. Mendiola, Andrew T. C. Tsin, Donald M. Allen, Astrid E. Cardona
Language: English
Subfield: Ophthalmology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,040
OpenAlex ID: W2051066258