Pathogenesis of Diabetic Retinopathy

Engerman, Ronald L.

doi:10.2337/diab.38.10.1203

Cited by 245 publications

(131 citation statements)

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“…Given the good correlation between plasma leptin concentra- tions and adiposity, the association between the degree of diabetic retinopathy and adiposity should be examined carefully. It is well recognized that hyperglycemia is one of the possible contributors to the development of diabetic retinopathy (2)(3)(4). In this regard, it is interesting to examine the degree of diabetic retinopathy in patients with lipoatrophic diabetes who have hyperglycemia but hypoleptinemia (27).…”

Section: Discussionmentioning

confidence: 99%

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Leptin Stimulates Ischemia-Induced Retinal Neovascularization

et al. 2004

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Section: Discussionmentioning

confidence: 99%

“…One of the possible contributors to the development of diabetic retinopathy is hyperglycemia, which leads to increased vasopermeability, endothelial cell proliferation, and neovascularization (2)(3)(4). Not all patients with poor control of diabetes over long periods of time, however, develop retinopathy, suggesting the involvement of other mechanisms.…”

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confidence: 99%

Leptin Stimulates Ischemia-Induced Retinal Neovascularization

et al. 2004

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“…[Diabetologia (2003) 46:409-415] Keywords Diabetic retinopathy, extracellular matrix, pericytes, endothelium, glucose, galactose, aminoguanidine, thiamine, glycation. and is observed in other forms of hyperhexosaemia, such as galactose-fed rats, which also develop a diabetic-like retinopathy [3,4]. The evolution of diabetic retinopathy is strongly influenced by qualitative and quantitative changes in the extracellular matrix (ECM) of the capillary basement membrane.…”

Section: Introductionmentioning

confidence: 99%

A study of capillary pericyte viability on extracellular matrix produced by endothelial cells in high glucose

et al. 2003

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Aims/hypothesis. Thickening of the basement membrane and selective loss of pericytes occur early in diabetic retinopathy. As we showed previously that pericyte adhesion is impaired on extracellular matrix produced by endothelial cells in high hexose concentrations, we aimed to verify if altered adhesion could influence pericyte viability and replication. Methods. Conditioned extracellular matrices were obtained by growing human umbilical vein endothelial cells in media containing 28 mmol/l D-glucose, with or without the inhibitors of protein glycation thiamine or aminoguanidine, and D-galactose or L-glucose up to 28 mmol/l. Having removed the endothelium, bovine retinal pericytes were grown on these matrices and, in separate experiments, on laminin, fibronectin or type IV collagen. Pericyte viability and replication were measured by cell counts and DNA synthesis after 7 days, cell cycle traversal after 2 days and apoptosis after 18 h, 2 days and 7 days.Results. Pericyte counts and DNA synthesis were reduced on matrices produced in high D-glucose and Dgalactose, whilst matrix obtained in L-glucose reduced DNA synthesis but not counts. Both thiamine and aminoguanidine corrected reduced pericyte viability when added to high D-glucose. Cell cycle and apoptosis were not affected by growing pericytes on different conditioned matrices. Laminin, fibronectin and type IV collagen did not modify pericyte replication. Conclusions/interpretations. Reduced pericyte counts could depend on impaired initial adhesion to the extracellular matrix produced by endothelium in high hexose concentrations, rather than impaired replication or viability. Altered cell-matrix interactions might facilitate pericyte dropout in diabetic retinopathy, independently of the effects of high glucose on pericyte replication. [Diabetologia (2003) 46:409-415] Keywords Diabetic retinopathy, extracellular matrix, pericytes, endothelium, glucose, galactose, aminoguanidine, thiamine, glycation. and is observed in other forms of hyperhexosaemia, such as galactose-fed rats, which also develop a diabetic-like retinopathy [3,4]. The evolution of diabetic retinopathy is strongly influenced by qualitative and quantitative changes in the extracellular matrix (ECM) of the capillary basement membrane. In particular, alterations of some ECM components were shown to influence the characteristics of endothelium [5] and ECM-associated growth factors [6], although the mechanisms are still unclear.Endothelium is likely to represent the major contributor to the synthesis of capillary ECM material. In particular, endothelial cells were found to increase their synthesis of type IV collagen and fibronectin Thickening of the basement membrane is an early event in the course of diabetic microangiopathy [1,2]

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“…During nonproliferative DR, the earliest visible sign of retinal damage results from abnormal permeability and/or nonperfusion of capillaries, leading to the formation of microaneurysms. 19,20 Abnormal capillary permeability results in the leaking of fluid and solutes into the surrounding retinal tissue, which collects around the macula; this is referred to as macular oedema (MO) and it threatens visual acuity. PDR develops following the occlusion of retinal capillaries leading to retinal ischaemia, which promotes the development of neovascularization, a process by which new blood vessels proliferate on the surface of the retina.…”

Section: Introductionmentioning

confidence: 99%

Epidemiology of diabetic retinopathy and macular oedema: a systematic review

Williams

Airey

Baxter

et al. 2004

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Aims To systematically review the literature on the prevalence and incidence of diabetic retinopathy (DR) and macular oedema (MO). Methods A search of the bibliographic databases (Medline, Embase, CINAHL) was conducted up to October 2001. Selected relevant studies were scrutinized and included in the review. Results A total of 359 studies were included. The studies were reported in nearly 100 different journals and in over 50 countries. The majority of the studies were US-based, with large studies such as the Wisconsin Epidemiologic Study of Diabetic Retinopathy dominating the literature. The studies were quite dated and highly heterogeneous in nature in terms of patient selection with variable inclusion criteria (age range, gender, diabetes duration and type, ethnicity, comorbidity, and DR status, assessment, and classification). Conclusions There are inconsistencies between epidemiological studies, and differences in study methods may contribute to conflicting reports of prevalence and incidence of DR and MO in diabetic populations. As new therapies for DR and its associated complications emerge, the need to capture and monitor new epidemiological data becomes increasingly important to be able to assess the impact and effectiveness of these therapies. Robust, longitudinal capture of patient data is, therefore, essential to evaluate the impact of current practice on the epidemiology of diabetic eye complications.

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Pathogenesis of Diabetic Retinopathy

Cited by 245 publications

References 0 publications

Leptin Stimulates Ischemia-Induced Retinal Neovascularization

Leptin Stimulates Ischemia-Induced Retinal Neovascularization

A study of capillary pericyte viability on extracellular matrix produced by endothelial cells in high glucose

Epidemiology of diabetic retinopathy and macular oedema: a systematic review

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