Microvascular lesions of diabetic retinopathy: clues towards understanding pathogenesis?

• Published in: Eye (London) Vol. 23; no. 7; pp. 1496 - 1508
• Main Authors: Curtis, T M, Gardiner, T A, Stitt, A W
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.07.2009; Nature Publishing Group
• Subjects: Biological and medical sciences; Diabetes Mellitus - physiopathology; Diabetes. Impaired glucose tolerance; Diabetic Retinopathy - physiopathology; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Hemodynamics; Humans; Hypoxia - etiology; Laboratory Medicine; Medical sciences; Medicine; Medicine & Public Health; Microcirculation - physiology; Miscellaneous; Ophthalmology; Pharmaceutical Sciences/Technology; Regional Blood Flow; Retinal Vessels - physiology; Retinopathies; review; Surgery; Surgical Oncology; hypoxia; ischaemia; diabetic retinopathy; diabetes; blood flow; haemodynamics; Endocrinopathy; Oxygen; Retinopathy; Pathogenesis; Diabetes mellitus; Cardiovascular disease; Blood flow; Microcirculation; Eye disease; Ischemia; Hypoxia; Hemodynamics; Lesion; Ophthalmology
• ISSN: 0950-222X; 1476-5454
• DOI: 10.1038/eye.2009.108

Retinopathy is a major complication of diabetes mellitus and this condition remains a leading cause of blindness in the working population of developed countries. As diabetic retinopathy progresses a range of neuroglial and microvascular abnormalities develop although it remains unclear how these pathologies relate to each other and their net contribution to retinal damage. From a haemodynamic perspective, evidence suggests that there is an early reduction in retinal perfusion before the onset of diabetic retinopathy followed by a gradual increase in blood flow as the complication progresses. The functional reduction in retinal blood flow observed during early diabetic retinopathy may be additive or synergistic to pro-inflammatory changes, leucostasis and vaso-occlusion and thus be intimately linked to the progressive ischaemic hypoxia and increased blood flow associated with later stages of the disease. In the current review a unifying framework is presented that explains how arteriolar dysfunction and haemodynamic changes may contribute to late stage microvascular pathology and vision loss in human diabetic retinopathy.