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Armstrong, Donald; Ueda, Toshihiko; Aljada, Ahmad; Browne, Richard W.; Fukuda, Shohei; Spengler, Robert N.; Chou, Richard C.; Hartnett, M. Elizabeth; Buch, P; Dandona, Paresh; Sasisekharan, Ram; Dorey, C. Kathleen

doi:10.1023/a:1009010628371

Cited by 61 publications

(4 citation statements)

References 53 publications

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“…Oxidative stress induced by hyperglycaemia is an important pathway of diabetic microvascular complications [103], and increasing evidence suggests that the correlation between hyperglycaemia, changes in the redox homeostasis, and oxidative stress is the key event in the pathogenesis of diabetic retinopathy [104–106]. It has been hypothesised that both the development and the progression of retinopathy result from increased oxidative species [107, 108]. …”

Section: Oxidative Stressmentioning

confidence: 99%

Pathophysiology of Diabetic Retinopathy

et al. 2013

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Diabetes is now regarded as an epidemic, with the population of patients expected to rise to 380 million by 2025. Tragically, this will lead to approximately 4 million people around the world losing their sight from diabetic retinopathy, the leading cause of blindness in patients aged 20 to 74 years. The risk of development and progression of diabetic retinopathy is closely associated with the type and duration of diabetes, blood glucose, blood pressure, and possibly lipids. Although landmark cross-sectional studies have confirmed the strong relationship between chronic hyperglycaemia and the development and progression of diabetic retinopathy, the underlying mechanism of how hyperglycaemia causes retinal microvascular damage remains unclear. Continued research worldwide has focussed on understanding the pathogenic mechanisms with the ultimate goal to prevent DR. The aim of this paper is to introduce the multiple interconnecting biochemical pathways that have been proposed and tested as key contributors in the development of DR, namely, increased polyol pathway, activation of protein kinase C (PKC), increased expression of growth factors such as vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1), haemodynamic changes, accelerated formation of advanced glycation endproducts (AGEs), oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and subclinical inflammation and capillary occlusion. New pharmacological therapies based on some of these underlying pathogenic mechanisms are also discussed.

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Section: Oxidative Stressmentioning

confidence: 99%

Pathophysiology of Diabetic Retinopathy

et al. 2013

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“…Increased levels of TNF- α have been demonstrated in proliferative retinopathies and in animal models of retinal NV [109–112]. These increased levels of TNF- α may be collaborating with VEGF to stimulate retinal NV.…”

Section: Cytokinesmentioning

confidence: 99%

Vitreous Mediators in Retinal Hypoxic Diseases

dell’Omo

Semeraro

Bamonte

et al. 2013

Mediators of Inflammation

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The causes of retinal hypoxia are many and varied. Under hypoxic conditions, a variety of soluble factors are secreted into the vitreous cavity including growth factors, cytokines, and chemokines. Cytokines, which usually serve as signals between neighboring cells, are involved in essentially every important biological process, including cell proliferation, inflammation, immunity, migration, fibrosis, tissue repair, and angiogenesis. Cytokines and chemokines are multifunctional mediators that can direct the recruitment of leukocytes to sites of inflammation, promote the process, enhance immune responses, and promote stem cell survival, development, and homeostasis. The modern particle-based flow cytometric analysis is more direct, stable and sensitive than the colorimetric readout of the conventional ELISA but, similar to ELISA, is influenced by vitreous hemorrhage, disruption of the blood-retina barrier, and high serum levels of a specific protein. Finding patterns in the expression of inflammatory cytokines specific to a particular disease can substantially contribute to the understanding of its basic mechanism and to the development of a targeted therapy.

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“…Vascular endothelial growth factor (VEGF) is considered to be a major factor in the breakdown of BRB [13]. However, other permeabilizing factors such as histamine, interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) have also been implicated [14][15][16]. VEGF is increased in the eyes of diabetic patients and diabetic rats at the early stages of DR, and this observation was correlated with increased vascular permeability [17][18][19].…”

Section: Blood-retinal Barrier Breakdown and Neovascularization: Antimentioning

confidence: 99%

Old and New Drug Targets in Diabetic Retinopathy: From Biochemical Changes to Inflammation and Neurodegeneration

Leal¹,

Santiago²,

Ambrósio

2005

CDTCNSND

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Diabetic Retinopathy (DR) is a major complication of diabetes and is a leading cause of blindness in western countries. DR has been considered a microvascular disease, and the blood-retinal barrier breakdown is a hallmark of this disease. The available treatments are scarce and not very effective. Despite the attempts to control blood glucose levels and blood pressure, many diabetic patients are affected by DR, which progresses to more severe forms of disease, where laser photocoagulation therapy is needed. DR has a huge psychological impact in patients and tremendous economic and social costs. Taking this into account, the scientific community is committed to find a treatment to DR. Understanding the cellular and molecular mechanisms underlying the pathogenesis of DR will facilitate the development of strategies to prevent, or at least to delay the progression of the disease. The involvement of the polyol pathway, advanced glycation end products, protein kinase C and oxidative stress in the pathogenesis of DR is well-documented, and several clinical trials have been conducted to test the efficacy of various drugs. More recent findings also demonstrate that DR has characteristics of chronic inflammatory disease and neurodegenerative disease, which increases the opportunity of intervention at the pharmacological level. This review presents past and recent evidences demonstrating the involvement of different molecules and processes in DR, and how different approaches and pharmacological tools have been used to prevent retinal cell dysfunction.

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Untitled

Cited by 61 publications

References 53 publications

Pathophysiology of Diabetic Retinopathy

Pathophysiology of Diabetic Retinopathy

Vitreous Mediators in Retinal Hypoxic Diseases

Old and New Drug Targets in Diabetic Retinopathy: From Biochemical Changes to Inflammation and Neurodegeneration

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