The significance of vascular and neural apoptosis to the pathology of diabetic retinopathy

Alistair J. Barber, Thomas W. Gardner, Steven F. Abcouwer

Research output: Contribution to journalReview articlepeer-review

363 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1156-1163
Number of pages8
JournalInvestigative Ophthalmology and Visual Science
Volume52
Issue number2
DOIs
StatePublished - Feb 2011

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Fingerprint

Dive into the research topics of 'The significance of vascular and neural apoptosis to the pathology of diabetic retinopathy'. Together they form a unique fingerprint.

Cite this