Angiotensin converting enzyme inhibiting therapy is associated with lower vitreous vascular endothelial growth factor concentrations in patients with proliferative diabetic retinopathy

Buggenum, I. M. Hogeboom van; Polak, B.C.P.; Reichert-Thoen, J. W.; Vries-Knoppert, W. A. E. J. De; Hinsbergh, Victor W.M. van; Tangelder, G. J.

doi:10.1007/s00125-001-0747-8

Cited by 69 publications

(29 citation statements)

References 22 publications

(35 reference statements)

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“…observation]. The IGF-1 trigger mechanism is apparently effective via vascular endothelial growth factor [2, 14, 15, 16]. It appears that this mechanism works in diabetic nephropathy, too [17].…”

Section: Discussionmentioning

confidence: 99%

Reversion of ‘Early Worsening’ of Diabetic Retinopathy by Deliberate Restoration of Poor Metabolic Control

Chantelau

Meyer-Schwickerath²

2003

Ophthalmologica

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Acutely lowering long-standing severe hyperglycaemia can trigger progression (‘early worsening’) of diabetic retinopathy, most likely by up-regulation of the circulating insulin-like growth factor 1 (IGF-1). This condition, also called ‘florid retinopathy’, rarely responds to standard laser coagulation treatment. In this retrospective report, 2 young patients with type 2 diabetes are described, in whom deliberate restoration of poor diabetes control reduced the serum IGF-1 levels and improved ‘early worsened’ diabetic retinopathy.

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Section: Discussionmentioning

confidence: 99%

Reversion of ‘Early Worsening’ of Diabetic Retinopathy by Deliberate Restoration of Poor Metabolic Control

Chantelau

Meyer-Schwickerath²

2003

Ophthalmologica

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“…In patients with proliferative diabetic retinopathy, huge levels of VEGF have been found in the eye fluid, indicating an important contribution of this angiogenic factor (Aiello et al 1994). Furthermore, the level of VEGF is lower in diabetes patients treated with angiotensinconverting enzyme (ACE) inhibitors suggesting that angiotensin 2 also contributes (Hogeboom et al 2002). Either diabetes itself or the hypoxia that results from endothelial and vascular injury may induce these factors.…”

Section: Altered Angiogenesis and Tissue Repairmentioning

confidence: 99%

Endothelial dysfunction and diabetes: roles of hyperglycemia, impaired insulin signaling and obesity

et al. 2008

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Endothelial dysfunction comprises a number of functional alterations in the vascular endothelium that are associated with diabetes and cardiovascular disease, including changes in vasoregulation, enhanced generation of reactive oxygen intermediates, inflammatory activation, and altered barrier function. Hyperglycemia is a characteristic feature of type 1 and type 2 diabetes and plays a pivotal role in diabetesassociated microvascular complications. Although hyperglycemia also contributes to the occurrence and progression of macrovascular disease (the major cause of death in type 2 diabetes), other factors such as dyslipidemia, hyperinsulinemia, and adipose-tissue-derived factors play a more dominant role. A mutual interaction between these factors and endothelial dysfunction occurs during the progression of the disease. We pay special attention to the possible involvement of endoplasmic reticulum stress (ER stress) and the role of obesity and adipose-derived adipokines as contributors to endothelial dysfunction in type 2 diabetes. The close interaction of adipocytes of perivascular adipose tissue with arteries and arterioles facilitates the exposure of their endothelial cells to adipokines, particularly if inflammation activates the adipose tissue, and thus affects vasoregulation and capillary recruitment in skeletal muscle. Hence, an initial dysfunction of endothelial cells underlies metabolic and vascular alterations that contribute to the development of type 2 diabetes.

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“…However, the association between the reninangiotensin system and the development and progression of diabetic retinopathy is not straightforward, and initial results looking at the influence of ACE inhibitors on diabetic retinopathy in normotensive diabetic subjects have had equivocal results. Two recent studies examining the relationship between vitreous and plasma VEGF concentrations and the use of ACE inhibitors demonstrated differing results (97,98). In one study, it was found that the use of ACE inhibitors decreased levels of vitreous VEGF, possibly protecting against the development of PDR, while circulating plasma VEGF levels were not affected by ACE inhibitors in the other.…”

Section: Management Of Impaired Renal Functionmentioning

confidence: 99%

Diabetic Retinopathy

et al. 2004

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Angiotensin converting enzyme inhibiting therapy is associated with lower vitreous vascular endothelial growth factor concentrations in patients with proliferative diabetic retinopathy

Cited by 69 publications

References 22 publications

Reversion of ‘Early Worsening’ of Diabetic Retinopathy by Deliberate Restoration of Poor Metabolic Control

Reversion of ‘Early Worsening’ of Diabetic Retinopathy by Deliberate Restoration of Poor Metabolic Control

Endothelial dysfunction and diabetes: roles of hyperglycemia, impaired insulin signaling and obesity

Diabetic Retinopathy

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