Hypertension Increases Retinal Inflammation in Experimental Diabetes: A Possible Mechanism for Aggravation of Diabetic Retinopathy by Hypertension

Silva, Kamila C.; Pinto, Clarice Maia Soares de Alcântara; Biswas, Subrata Kumar; Faria, José B. Lopes de; Faria, Jacqueline M. Lopes de

doi:10.1080/02713680701435391

Cited by 40 publications

(24 citation statements)

References 46 publications

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“…We have demonstrated that the concomitance of both diabetes and hypertension leads to earlier and more pronounced retinal inflammatory alterations characterized by increased expression levels of ICAM-1, VEGF and NF-kB p65 in the retina when compared with those of normotensive diabetic rats. 92 Further corroborating the contribution of hypertension to retinal damage in diabetic SHR, we have demonstrated that anti-hypertensive treatment either with losartan (an AT1 receptor blocker, ARB) or with triple therapies (hydralazine, reserpine and hydrochlorothiazide) abolished these effects. 84 In the retina, a number of studies have shown that there is an increase in oxidative markers after the induction of DM, 67,[93][94][95] but the concomitance of diabetes and hypertension evoked earlier oxidative retinal damage characterized by an increase in nitrotyrosine and 8-OHdG in retinal tissue from short-term STZ-induced DM in SHRs.…”

Section: Inflammation and Oxidative Stress As The Underlying Mechanissupporting

confidence: 65%

The contribution of hypertension to diabetic nephropathy and retinopathy: the role of inflammation and oxidative stress

2011

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Diabetes and hypertension frequently coexist and constitute the most notorious combination for the pathogenesis of diabetic nephropathy and retinopathy. Large clinical trials have clearly demonstrated that tight control of glycemia and/or blood pressure significantly reduces the incidence and progression of diabetic retinopathy (DR) and nephropathy. However, the mechanism by which hypertension interacts with diabetes to induce and/or exacerbate nephropathy and retinopathy is very unclear. Substantial evidence implicates the involvement of chronic inflammation and oxidative stress in the pathogenesis of DR and nephropathy. In addition, hypertension causes oxidative stress and inflammation in the kidney and retina. In the present review, we summarized data obtained from our research along with those from other groups to better understand the role of hypertension in the pathogenesis of diabetic nephropathy and retinopathy. It is suggested that oxidative stress and inflammation may be common denominators of kidney and retinal damage in the concomitant presence of diabetes and hypertension.

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Section: Inflammation and Oxidative Stress As The Underlying Mechanissupporting

confidence: 65%

The contribution of hypertension to diabetic nephropathy and retinopathy: the role of inflammation and oxidative stress

2011

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“…A number of studies utilized immunohistochemistry to examine microglia, or to be more precise, cells expressing myeloid lineage or monocytic markers, within diabetic and control retinas. These studies reported increased numbers of microglia in retinas of rats made diabetic with STZ [103,[172][173][174][175]. Many of these cells were less ramified than normal retinal microglia or were even amoeboid in shape [103,172,175].…”

Section: Possible Causes Of Retinal Neuroinflammation In Drmentioning

confidence: 99%

Angiogenic Factors and Cytokines in Diabetic Retinopathy

Abcouwer¹

2011

J Clin Cell Immunol

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Diabetic retinopathy (DR) is a sight-threatening complication of both type-1 and type-2 diabetes. The recent success of treatments inhibiting the function of vascular endothelial growth factor (VEGF) demonstrates that specific targeting of a growth factor responsible for vascular permeability and growth is an effective means of treating DRtargets involved in the control of retinal vascular function. However, additional treatment options and preventative measures are still needed and these require a greater understanding of the pathological mechanisms leading to the disturbance of retinal tissue homeostasis in DR. Although severe DR can be treated as a vascular disease, abundant data suggests that inflammation is also occurring in the diabetic retina.Thus, anti-inflammatory therapies may also be useful for treatment and prevention of DR. Herein, the evidence for altered expression of angiogenic factors and cytokines in DR is reviewed and possible mechanisms by which the expression of VEGF and cytokines may be increased in the diabetic retina are examined. In addition, the potential role for microglial activation in diabetic retinal neuroinflammation is explored.

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“…A number of studies have utilized IHC to examine microglial numbers and shapes in diabetic versus control retinas. In rats made diabetic with STZ, there are increased numbers of microglia, or to be more precise, cells reactive with markers to monocytic proteins [39,[51][52][53][54][55]. Many of these cells are less ramified than normal retinal microglia or are even amoeboid in shape [39,54,55].…”

Section: Microglial Activation In Diabetic Retinopathymentioning

confidence: 99%