Demonstration of renin mRNA, angiotensinogen mRNA, and angiotensin converting enzyme mRNA expression in the human eye: evidence for an intraocular renin-angiotensin system.

Wagner, Juergen; Danser, A.H. Jan; Derkx, F. H. M.; Jong, T V de; Paul, Martin; Mullins, JJ; Schalekamp, M. A. D. H.; Ganten, Detlev

doi:10.1136/bjo.80.2.159

Cited by 253 publications

(205 citation statements)

References 20 publications

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“…Over 2 years, lisinopril reduced the progression of DR by 50% (95% CI, 28-89%) and progression to proliferative DR by 80%. [41] This study concluded that ACE inhibitors may provide additional benefits in DR progression independent of BP lowering effect. [48] While the EUCLID study suggested beneÞ cial effects of ACE inhibitors, UKPDS [37][38][39] and the ABCD study could not confirm the superiority of ACE inhibitors over other antihypertensives.…”

Section: T a B L E 1 A M E R I C A N D I A B E T E S A S S O C I A mentioning

confidence: 71%

“…[39] Understanding the role of reninangiotensin system (RAS) in DR Preliminary studies have shown that angiotensin converting enzyme (ACE) is locally produced by endothelial cells of retinal vessels and retinal pigment cells. [40,41] The retinal ACE expression causes adverse changes in retinal blood ß ow and vascular structure. [42] A small clinical study also showed that subjects treated with ACE inhibitors had relatively lower levels of vitreous VEGF than those not on ACE inhibitor treatment [43] indicating that the adverse effects of retinal ACE expression may be mediated by potentiation of VEGF activity.…”

Section: T a B L E 1 A M E R I C A N D I A B E T E S A S S O C I A mentioning

confidence: 99%

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Diabetic retinopathy: A comprehensive review

Shah¹

2008

Indian J Med Sci

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Section: T a B L E 1 A M E R I C A N D I A B E T E S A S S O C I A mentioning

confidence: 71%

Section: T a B L E 1 A M E R I C A N D I A B E T E S A S S O C I A mentioning

confidence: 99%

Diabetic retinopathy: A comprehensive review

Shah¹

2008

Indian J Med Sci

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“…The reninangiotensin system (RAS) has an important role in regulation of electrolyte balance, vasoconstriction, and vascular remodeling. Local renin-angiotensin regulation is present in the eye [139]. The role of the RAS in diabetic retinopathy has not been as well studied as that in the kidney and nephropathy; however, several studies including the Renin-Angiotensin System Study (RASS), Daily-Dose Consensus Interferon and Ribavirin: Efficacy of Combined Therapy (DIRECT) trial, and the ADVANCE Retinal Measurements (AdRem) have provided evidence that RAS inhibition may also be beneficial in diabetic retinopathy [140,141].…”

Section: Role Of the Renin-angiotensin System Its Inhibitors And Usmentioning

confidence: 99%

Molecular mechanisms of Diabetic Retinopathy, general preventive strategies and novel therapeutic targets

Safi¹,

Qvist²,

Kumar³

et al. 2013

Exp Clin Endocrinol Diabetes

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The growing number of people with diabetes worldwide suggests that diabetic retinopathy (DR) and diabetic macular edema (DME) will continue to be sight threatening factors. The pathogenesis of diabetic retinopathy is a widespread cause of visual impairment in the world and a range of hyperglycemia-linked pathways have been implicated in the initiation and progression of this condition. Despite understanding the polyol pathway flux, activation of protein kinase C (KPC) isoforms, increased hexosamine pathway flux, and increased advanced glycation end-product (AGE) formation, pathogenic mechanisms underlying diabetes induced vision loss are not fully understood. The purpose of this paper is to review molecular mechanisms that regulate cell survival and apoptosis of retinal cells and discuss new and exciting therapeutic targets with comparison to the old and inefficient preventive strategies. This review highlights the recent advancements in understanding hyperglycemia-induced biochemical and molecular alterations, systemic metabolic factors, and aberrant activation of signaling cascades that ultimately lead to activation of a number of transcription factors causing functional and structural damage to retinal cells. It also reviews the established interventions and emerging molecular targets to avert diabetic retinopathy and its associated risk factors.

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“…One such pathway is the renin-angiotensin system (RAS) as there is evidence that a local RAS including renin exists within the retina [2][3][4], and that prorenin is elevated in the plasma and vitreous humour of patients with proliferative diabetic retinopathy [5,6]. Furthermore, experimental studies indicate that ACE inhibition and type 1 angiotensin receptor blockade (ARB) are protective in models of retinopathy [7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Aliskiren reduces vascular pathology in diabetic retinopathy and oxygen-induced retinopathy in the transgenic (mRen-2)27 rat

et al. 2011

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Aim/hypothesis We examined whether the renin inhibitor, aliskiren, provides similar or greater protection than ACE inhibition from non-proliferative diabetic retinopathy and from the proliferative neoangiogenesis of oxygen-induced retinopathy. Methods Transgenic (mRen-2)27 rats, which overexpress mouse renin and angiotensin in extra-renal tissues, were studied. For diabetic studies, non-diabetic, diabetic (streptozotocin, 55 mg/kg), diabetic + aliskiren (10 mg kg −1 day −1 , pump), or diabetic + lisinopril (10 mg kg −1 day −1 , drinking water) rats were evaluated over 16 weeks. For oxygeninduced retinopathy studies, rats were exposed to 80% oxygen (22 h/day) from postnatal days 0 to 11, and then room air from postnatal days 12 to 18. Aliskiren (10 or 30 mg kg −1 day −1 , pump) or lisinopril (10 mg kg −1 day −1 , drinking water) was administered during retinopathy development between postnatal days 12 and 18. Results Systolic BP in diabetic (mRen-2)27 rats was reduced with 10 mg kg −1 day −1 aliskiren, but only lisinopril normalised systolic blood pressure. In diabetic (mRen-2)27 rats, 10 mg kg −1 day −1 aliskiren and lisinopril reduced retinal acellular capillaries and leucostasis to non-diabetic levels. In oxygen-induced retinopathy, neoangiogenesis and retinal inflammation (leucostasis, ED-1 immunolabelling) were partially reduced by 10 mg kg −1 day −1 aliskiren and normalised by 30 mg kg −1 day −1 aliskiren, whereas lisinopril normalised neoangiogenesis and reduced leucostasis and ED-1 immunolabelling. Aliskiren and lisinopril normalised retinal vascular endothelial growth factor expression; however, only aliskiren reduced intercellular adhesion molecule-1 to control levels. Conclusions/interpretation Aliskiren provided similar or greater retinal protection than ACE inhibition and may be a potential treatment for diabetic retinopathy.

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Demonstration of renin mRNA, angiotensinogen mRNA, and angiotensin converting enzyme mRNA expression in the human eye: evidence for an intraocular renin-angiotensin system.

Cited by 253 publications

References 20 publications

Diabetic retinopathy: A comprehensive review

Diabetic retinopathy: A comprehensive review

Molecular mechanisms of Diabetic Retinopathy, general preventive strategies and novel therapeutic targets

Aliskiren reduces vascular pathology in diabetic retinopathy and oxygen-induced retinopathy in the transgenic (mRen-2)27 rat

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