Inflammation and diabetic nephropathy

Mora, Carmen; Navarro, Juan F.

doi:10.1007/s11892-006-0080-1

Cited by 174 publications

(127 citation statements)

References 74 publications

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“…21 Hemodialysis affects both oxidative stress and cellular inflammation. Various studies showed the increasing of the oxidative stress and the reduction of antioxidant defenses in patients with chronic renal failure.…”

Section: Discussionmentioning

confidence: 99%

Determination of oxidative stress and cellular inflammation in patients with diabetic nephropathy and non-diabetic nephropathy being administered hemodialysis treatment due to chronic renal failure

et al. 2014

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Objectives: We aimed to evaluate oxidative stress , malondialdehyde (MDA)] endothelial damage [asymmetric dimethylarginine (ADMA)] and markers of cellular inflammation [interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-a), neopterin (NP) and high-sensitivity C-reactive protein (hsCRP)] in patients with diabetic nephropathy (DN) and non-diabetic nephropathy who were being administered hemodialysis treatment because of chronic renal failure. Methods: In determining 8-OHdG, IL-6 and TNF-a levels, Enzyme-Linked Immuno-Sorbent Assay method was used. Serum MDA, ADMA and NP levels were determined by using high performance liquid chromatography (HPLC). And hs-CRP values were measured with nephelometric method. Results: Serum 8-OHdG and MDA levels were found statistically to have increased when compared with those of the control group in patients groups after dialysis. However, serum ADMA and neopterin levels were observed statistically to have decreased when compared with those of the control group in patients groups after dialysis. But, decreases on ADMA and neopterin levels are still much higher than those of control. IL-6 and TNF-a levels were found to have increased when compared with those of control group in patients groups before dialysis. Conclusion: The oxidative stress in patients with DN, who were being treated with hemodialysis due to chronic renal failure, was higher than that of non-DN patients who were being treated with hemodialysis. In contrast with this, inflammation occurring in non-DN patients was found to have been higher than that of in patients with DN.

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Section: Discussionmentioning

confidence: 99%

Determination of oxidative stress and cellular inflammation in patients with diabetic nephropathy and non-diabetic nephropathy being administered hemodialysis treatment due to chronic renal failure

et al. 2014

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“…DN was considered to be a nonimmune disease. Nevertheless, it has been shown recently that inflammation is crucial for the development of microvascular complications of DM, including nephr opathy (Mora and Navarro, 2006;Ortiz-Munoz et al, 2010).…”

Section: Pathophysiological Features Of Diabetic Nephro-pathymentioning

confidence: 99%

“…Moreover, it has been proved that IL-1beta, IL-6 and TNF-alpha are relevant for the developme nt of DN (Mocan et al, 2006;Mora and Navarro, 2006). IL-1beta and IL-6 increase vascular endothelial permeability and alter ECM dynamics at both the mesangial and podocyte levels, contributing to interstitial infi ltrates, glomerular basement membrane thickening, mesangial expansion, and tubula r atrophy (Pecoits-Filho et al, 2002;Dalla et al, 2005).…”

Section: Pathophysiological Features Of Diabetic Nephro-pathymentioning

confidence: 99%

MSC transplantation: a promising therapeutic strategy to manage the onset and progression of diabetic nephropathy

Ezquer

Arango-Rodríguez

et al. 2012

Biol. Res.

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Currently, one of the main threats to public health is diabetes mellitus. Its most detrimental complication is diabetic nephropathy (DN), a clinical syndrome associated with kidney damage and an increased risk of cardiovascular disease. Irrespective of the type of diabetes, DN follows a well-known temporal course. The earliest detectable signs are microalbuminuria and histopathological changes including extracellular matrix deposition, glomerular basement membrane thickening, glomerular and mesangial expansion. Later on macroalbuminuria appears, followed by a progressive decline in glomerular fi ltration rate and the loss of glomerular podocytes, tubulointerstitial fi brosis, glomerulosclerosis and arteriolar hyalinosis. Tight glycemic and hypertension controls remain the key factors for preventing or arresting the progression of DN. Nevertheless, despite considerable educational eff ort to control the disease, a signifi cant number of patients not only develop DN, but also progress to chronic kidney disease. Therefore, the availability of a strategy aimed to prevent, delay or revert DN would be highly desirable. In this article, we review the pathophysiological features of DN and the therapeutic mechanisms of multipotent mesenchymal stromal cells, also referred to as mesenchymal stem cells (MSCs). The perfect match between them, together with encouraging pre-clinical data available, allow us to support the notion that MSC transplantation is a promising therapeutic strategy to manage DN onset and progression, not only because of the safety of this procedure, but mainly because of the renoprotective potential of MSCs.

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“…Augmented inflammation is a hallmark of diabetes, 17,18 and this proinflammatory state plays a critical role in the development and progression of DN. 10,19,20 Elements of the diabetic milieu, such as hyperglycemia and advanced glycation endproducts are thought to play an important role in creating a proinflammatory environment in both peripheral circulation and renal tissues. 10,14,21,22 Moreover, the initial renal glomerular dysfunction is thought to result in macrophage infiltration due to increased expression of inflammatory adhesion and chemoattractant proteins.…”

mentioning

confidence: 99%

Anti-Inflammatory Role of MicroRNA-146a in the Pathogenesis of Diabetic Nephropathy

Bhatt

Lanting

Jia

et al. 2015

JASN

158

130

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Inflammation has a critical role in the pathogenesis of diabetic complications, including diabetic nephropathy (DN). MicroRNAs have recently emerged as important regulators of DN. However, the role of microRNAs in the regulation of inflammation during DN is poorly understood. Here, we examined the in vivo role of microRNA-146a (miR-146a), a known anti-inflammatory microRNA, in the pathogenesis of DN. In a model of streptozotocin-induced diabetes, miR-146a 2/2 mice showed significantly exacerbated proteinuria, renal macrophage infiltration, glomerular hypertrophy, and fibrosis relative to the respective levels in control wild-type mice. Diabetes-induced upregulation of proinflammatory and profibrotic genes was significantly greater in the kidneys of miR-146a 2/2 than in the kidneys of wild-type mice. Notably, miR146a expression increased in both peritoneal and intrarenal macrophages in diabetic wild-type mice. Mechanistically, miR-146a deficiency during diabetes led to increased expression of M1 activation markers and suppression of M2 markers in macrophages. Concomitant with increased expression of proinflammatory cytokines, such as IL-1b and IL-18, markers of inflammasome activation also increased in the macrophages of diabetic miR-146a 2/2 mice. These studies suggest that in early DN, miR-146a upregulation exerts a protective effect by downregulating target inflammation-related genes, resulting in suppression of proinflammatory and inflammasome gene activation. Loss of this protective mechanism in miR-146a 2/2 mice leads to accelerated DN. Taken together, these results identify miR-146a as a novel anti-inflammatory noncoding RNA modulator of DN. 27: 227727: -228827: , 201627: . doi: 10.1681 Diabetic nephropathy (DN) is the leading cause of CKD and ESRD. 1-6 Development and progression of DN involve a complex interplay among metabolic, hemodynamic, growth, and inflammatory factors. 1,3,[7][8][9][10][11][12][13] The progressive decline in renal function during DN is a result of a multitude of pathologic changes in the kidneys, including glomerular and tubular hypertrophy, macrophage infiltration, extracellular matrix (ECM) accumulation in multiple renal cells, mesangial expansion, endothelial dysfunction, and podocyte injury. 1,3,[7][8][9][10][11][12][14][15][16] These pathologic changes clinically manifest as proteinuria and a steady deterioration in GFR. 3,4,16 Identification of molecular pathways that contribute to the pathophysiology of DN is imperative for the development of new therapeutic strategies. J Am Soc NephrolConversely, identification of factors that exert adaptive and protective roles in the early stages of DN can be exploited to prevent progression to ESRD.

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Inflammation and diabetic nephropathy

Cited by 174 publications

References 74 publications

Determination of oxidative stress and cellular inflammation in patients with diabetic nephropathy and non-diabetic nephropathy being administered hemodialysis treatment due to chronic renal failure

Determination of oxidative stress and cellular inflammation in patients with diabetic nephropathy and non-diabetic nephropathy being administered hemodialysis treatment due to chronic renal failure

MSC transplantation: a promising therapeutic strategy to manage the onset and progression of diabetic nephropathy

Anti-Inflammatory Role of MicroRNA-146a in the Pathogenesis of Diabetic Nephropathy

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