Clinical significance of inflammatory and fibrogenic cytokines in diabetic nephropathy

Mesallamy, Hala O El; Ahmed, Hanaa H.; Bassyouni, Atef; Ahmed, Amira

doi:10.1016/j.clinbiochem.2012.02.021

Cited by 42 publications

(31 citation statements)

References 32 publications

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“…It's demonstrated that CTGF play a key role in DN caused by renal interstitial fibrosis and glomerulosclerosis, and could be a major cause of kidney damage in diabetes [5]. Urinary level of MCP-1 was observed to be significantly increased and was found to correlate with the degree of renal interstitial fibrosis and tubular atrophy [6]. Additionally, it was confirmed that urinary CTGF level could act as a sensitive early indicator of renal injury.…”

Section: Discussionsupporting

confidence: 52%

Effects of Triptergium Glycosides on Expressions of MCP- 1 and CTGF in Rats with Early Diabetic Nephropathy

Zhang¹,

Zhang²,

Yin³

et al. 2016

Trop. J. Pharm Res

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Section: Discussionsupporting

confidence: 52%

Effects of Triptergium Glycosides on Expressions of MCP- 1 and CTGF in Rats with Early Diabetic Nephropathy

Zhang¹,

Zhang²,

Yin³

et al. 2016

Trop. J. Pharm Res

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“…As we can see several kidney structures are susceptible to hyperglycemia, and this metabolic change cause organ damage due to several cellular via including genetic activation and expression, advanced glycation end products generation, polyol pathway activation, abnormal protein kinase activation (PKC), raise of oxidative stress and the molecules that act as growth factors, transcription factors and others [4,8] .…”

Section: Physiopathologymentioning

confidence: 99%

“…DN is characterized by glomerular hypertrophy, thickness of basement, tubular and glomerular membranes and accumulation of extracellular matrix in these membranes that finally cause tubulointerstitial and glomerular fibrosis and sclerosis [2,6,8] . As we can see several kidney structures are susceptible to hyperglycemia, and this metabolic change cause organ damage due to several cellular via including genetic activation and expression, advanced glycation end products generation, polyol pathway activation, abnormal protein kinase activation (PKC), raise of oxidative stress and the molecules that act as growth factors, transcription factors and others [4,8] .…”

Section: Physiopathologymentioning

confidence: 99%

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Diabetic nephropathy and inflammation

Durán-Salgado¹

2014

WJD

341

234

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Diabetic nephropathy (DN) is the leading cause of end-stage renal failure worldwide. Besides, diabetic nephropathy is associated with cardiovascular disease, and increases mortality of diabetic patients. Several factors are involved in the pathophysiology of DN, including metabolic and hemodynamic alterations, oxidative stress, and activation of the renin-angiotensin system. In recent years, new pathways involved in the development and progression of diabetic kidney disease have been elucidated; accumulated data have emphasized the critical role of inflammation in the pathogenesis of diabetic nephropathy. Expression of cell adhesion molecules, growth factors, chemokines and pro-inflammatory cytokines are increased in the renal tissues of diabetic patients, and serum and urinary levels of cytokines and cell adhesion molecules, correlated with albuminuria. In this paper we review the role of inflammation in the development of diabetic nephropathy, discussing some of the major inflammatory cytokines involved in the pathogenesis of diabetic nephropathy, including the role of adipokines, and take part in other mediators of inflammation, as adhesion molecules.

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“…Transforming growth factor (TGF)-β1 has been shown to be a potent growth factor that has a pivotal role in renal fibrogenesis and induces various biological effects via numerous signal transduction pathways (8,13,14). At present, TGF-β1 is recognized as the major cytokine responsible for the ECM pathology that accompanies DN (15). The mitogen-activated protein kinase (MAPK) signaling pathway is one of the most important signal transduction pathways and is found widely in cells (16).…”

Section: Introductionmentioning

confidence: 99%

Allicin inhibits tubular epithelial-myofibroblast transdifferentiation under high glucose conditions in vitro

Huang

Zheng

Dong

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Previous studies have suggested that tubular epithelial-mesenchymal transition (EMT) is an important event in renal tubulointerstitial fibrosis, which is a clinical characteristic of diabetic nephropathy. The present study aimed to investigate the effect of allicin, the major biological active component of garlic, on the EMT of a human renal proximal tubular epithelial cell line (HK-2) cultured under high glucose concentrations. HK-2 cells were exposed for 48 h to 5.5 or 25 mmol/l D-glucose, 25 mmol/l D-glucose plus allicin (2.5, 5, 10 or 20 µg/ml) or 25 mmol/l D-glucose plus 20 µmol/l PD98059, a selective inhibitor of the mitogen activated protein kinase/extracellular signal-regulated kinase (ERK) signaling pathway. The EMT of HK-2 cells was assessed by analyzing the protein expression of E-cadherin, α-smooth muscle actin (α-SMA), vimentin and collagen I via immunocytochemistry. In addition, reverse transcription-quantitative polymerase chain reaction and western blotting were used to detect the expression levels of transforming growth factor (TGF)-β1 and phosphorylated (p)-ERK1/2. Marked morphological changes were observed in HK-2 cells cultured under high glucose conditions, and these changes were abrogated by simultaneous incubation with allicin and PD98059. The expression levels of α-SMA, vimentin and collagen I were significantly increased in HK-2 cells cultured under high glucose conditions, as compared with those cultured under normal glucose conditions (P<0.01). Conversely, the expression levels of E-cadherin were significantly decreased upon stimulation with high glucose (P<0.01). Furthermore, the expression levels of TGF-β1 and p-ERK1/2 were significantly upregulated in HK-2 cells cultured under high glucose conditions, as compared with those cultured under normal glucose conditions (P<0.05).Allicin partially reversed the high-glucose-induced increase in α-SMA, vimentin and collagen I expression (P<0.01 at 20 µg/ml), increased the expression of E-cadherin, and significantly downregulated the high glucose-induced expression of TGF-β1 and p-ERK1/2 in a dose-dependent manner (P<0.05). The results of the present study suggested that high glucose concentrations induced the EMT of HK-2 cells, and that allicin was able to inhibit the EMT, potentially via regulation of the ERK1/2-TGF-β1 signaling pathway. IntroductionTubulointerstitial fibrosis, which is considered the final common pathway of progressive kidney diseases and eventually leads to end-stage renal disease, is a result of the tubular epithelial-to-mesenchymal transition (EMT) and excessive accumulation of extracellular matrix (ECM) that characterize the majority of chronic kidney diseases, including diabetic nephropathy (DN) (1). Previous studies have demonstrated that high glucose conditions induce the EMT in renal proximal tubular cells in vitro and in vivo (2-5). In addition, it has been reported that myofibroblast formation is a critical step in the pathogenesis of tubulointerstitial fibrosis, and it has been shown to be a key step in...

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Clinical significance of inflammatory and fibrogenic cytokines in diabetic nephropathy

Cited by 42 publications

References 32 publications

Effects of Triptergium Glycosides on Expressions of MCP- 1 and CTGF in Rats with Early Diabetic Nephropathy

Effects of Triptergium Glycosides on Expressions of MCP- 1 and CTGF in Rats with Early Diabetic Nephropathy

Diabetic nephropathy and inflammation

Allicin inhibits tubular epithelial-myofibroblast transdifferentiation under high glucose conditions in vitro

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