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Publication
The significance of vascular and neural apoptosis to the pathology of diabetic
retinopathy.
Authors
Barber AJ, Gardner TW, Abcouwer SF
Submitted By
Steven Abcouwer on 3/17/2014
Status
Published
Journal
Investigative ophthalmology & visual science
Year
2011
Date Published
2/1/2011
Volume : Pages
52 : 1156 - 1163
PubMed Reference
21357409
Abstract
The most striking features of diabetic retinopathy are the vascular
abnormalities that are apparent by fundus examination. There is also strong
evidence that diabetes causes apoptosis of neural and vascular cells in the
retina. Thus, there is good reason to define diabetic retinopathy as a form of
chronic neurovascular degeneration. In keeping with the gradual onset of
retinopathy in humans, the rate of cell loss in the animal models is insidious,
even in uncontrolled diabetes. This is not surprising given that a sustained
high rate of cell loss without regeneration would soon lead to catastrophic
tissue destruction. The consequences of ongoing cell death are difficult to
detect, and even the quantification of cumulative cell loss requires painstaking
histology and microscopy. This subtle cell loss raises the issue of the
relevance of the phenomenon to the progression of diabetic retinopathy and the
ultimate loss of vision. Neuronal function may be compromised in advance of
apoptosis, contributing to an early deterioration of vision. Here we review some
of the evidence supporting apoptotic cell death as a contributing mechanism of
diabetic retinopathy, explore some of the potential causes, and discuss the
potential links between apoptosis and loss of visual function in diabetic
retinopathy.
Investigators with authorship
Name
Institution
Steven Abcouwer
University of Michigan-Ann Arbor
Alistair Barber
Pennsylvania State University-Penn State College of Medicine
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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