NF-κB in inflammation and renal diseases

Zhang, Haisong; Sun, Shao Cong

doi:10.1186/s13578-015-0056-4

Cited by 297 publications

(219 citation statements)

References 163 publications

(202 reference statements)

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“…Many of these cytokines and chemokines are induced by hyperglycemia and are known to be regulated by NF-κB. The activation of NF-κB has important consequences in mediating monocyte and macrophage activation in the pathogenesis of DKD [31] . In streptozotocin-induced diabetic animals, NF-κB activation has been reported in kidney cortical tissues [32] .…”

Section: Discussionmentioning

confidence: 99%

Role of Glycyrrhizin in the Reduction of Inflammation in Diabetic Kidney Disease

Thakur

Nargis

González

et al. 2017

Nephron

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Background: Diabetic kidney disease (DKD) is one of the most debilitating complications of type 2 diabetes. Recent evidence suggests chronic inflammation to be one of the causal factors of DKD. The mechanisms entailed are not completely elucidated except that a variety of cytokines play a major role in this process. High mobility group box 1 (HMGB1) is a pro-inflammatory toll-like receptor-4 (TLR4)-binding cytokine that is involved in inflammation-associated gene expression. This investigation was designed to assess the involvement of HMGB1, TLR-4, and nuclear factor (NF)-κB in the development of DKD and to evaluate that whether blocking HMGB1 by its natural inhibitor Glycyrrhizin (GLC) can reduce the progression of the disease. Methods: Studies were carried out in 8-10-weeks old Zucker diabetic fatty (ZDF) and lean, age- and gender-matched rats. At 10 weeks of age, ZDF rats as compared to controls, showed hyperglycemia, without proteinuria. After 8-10 weeks of the development of diabetes, ZDF animals that showed proteinuria were treated with GLC for 4 weeks. In addition, normal rat kidney (NRK-52E) cells with epithelial-like morphology were comparatively treated with GLC under hyperglycemic condition in vitro. Results: Substantial increase in the expression of HMGB1, TLR4, and NF-κB in vivo and in vitro under hyperglycemic conditions was observed as compared to normoglycemic conditions. The overexpression of HMGB1, TLR4, NF-κB, and glomerular injury marker nestin was significantly ameliorated by GLC administration. Conclusion: Our findings suggest that hyperglycemia-induced HMGB1 activation in ZDF rats may contribute to the progression of DKD.

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Section: Discussionmentioning

confidence: 99%

Role of Glycyrrhizin in the Reduction of Inflammation in Diabetic Kidney Disease

Thakur

Nargis

González

et al. 2017

Nephron

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“…It mediates the transcriptional induction of various proinflammatory cytokines, such as TNF-a, IL-1, and IL-6, as well as a number of chemokines (Zhang and Sun, 2015). IL-6 is a pleiotropic proinflammatory cytokine.…”

Section: Discussionmentioning

confidence: 99%

Contrast Media-Induced Renal Inflammation Is Mediated Through HMGB1 and Its Receptors in Human Tubular Cells

Guan

Chen

Zuo

et al. 2017

DNA and Cell Biology

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With the rapid development of imaging diagnosis and interventional therapy, contrast media (CM) are widely used in clinics. However, contrast-induced nephropathy (CIN) is the third leading cause of hospital-acquired acute renal failure accounting for 10-12% of all causes of hospital-acquired renal failure. Recent study found that inflammation may participate in the pathogenesis of CIN, but the role of it remains unclear. HK-2 cells were treated with Iohexol, Urografin, and mannitol. Two types of CM increased the release of HMGB1 in cell supernatant accompanied by increased expression of TLR2 and CXCR4. Iohexol and Urografin also caused a significant increase in NF-κB followed by the release of IL-6 and MCP-1. To clarify the role of HMGB1, TLR2, and CXCR4, glycyrrhizin, anti-TLR2-IgG, and AMD3100 were used to inhibit HMGB1, TLR2, and CXCR4, respectively. Significant decrease in the expression of TLR2, CXCR4, nuclear NF-κB, and the release of IL-6 and MCP-1 were observed. These results indicate that TLR2 and CXCR4 signaling are involved in CM-induced HK-2 cell injury model in an HMGB1-dependent pathway, which may provide a new target for the prevention and the treatment of CIN.

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“…The non-canonical NF-κB pathway has been implicated in the pathogenesis of IgA nephropathy, a leading cause of primary glomerulonephritis kidney diseases, which are characterized by aberrant production of glycosylated IgA and the deposition of IgA-immune complexes in kidney glomeruli 153 . Studies of mouse models suggest that dysregulated non-canonical NF-κB pathway activation in B cells (owing to the loss of the negative regulator TBK1) is associated with elevated serum levels of IgA and nephropathy-like disease symptoms, including antibody deposition in kidney glomeruli and signs of kidney dysfunction 70 .…”

Section: Role In Inflammatory Diseasesmentioning

confidence: 99%

“…Similar pathological phenotypes have been detected in transgenic mice that overexpress BAFF in B cells 154 . An increasing number of studies also show that non-canonical NF-κB signalling in kidney cells can regulate inflammation when activated by TNF-like weak inducer of apoptosis (TWEAK), a TNF superfamily member implicated in the pathogenesis of kidney diseases 153,155 . Elevated expression of TWEAK and its receptor, FN14, has been detected in patients with kidney diseases and in animal models of kidney injury, and it has been implicated in the pathogenesis of kidney diseases 155 .…”

Section: Role In Inflammatory Diseasesmentioning

confidence: 99%

The non-canonical NF-κB pathway in immunity and inflammation

2017

Self Cite

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The nuclear factor-κB (NF-κB) family of transcription factors is activated by canonical and non-canonical signalling pathways, which differ in both signalling components and biological functions. Recent studies have revealed important roles for the non-canonical NF-κB pathway in regulating different aspects of immune functions. Defects in non-canonical NF-κB signalling are associated with severe immune deficiencies, whereas dysregulated activation of this pathway contributes to the pathogenesis of various autoimmune and inflammatory diseases. Here we review the signalling mechanisms and the biological function of the non-canonical NF-κB pathway. We also discuss recent progress in elucidating the molecular mechanisms regulating non-canonical NF-κB pathway activation, which may provide new opportunities for therapeutic strategies.

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NF-κB in inflammation and renal diseases

Cited by 297 publications

References 163 publications

Role of Glycyrrhizin in the Reduction of Inflammation in Diabetic Kidney Disease

Role of Glycyrrhizin in the Reduction of Inflammation in Diabetic Kidney Disease

Contrast Media-Induced Renal Inflammation Is Mediated Through HMGB1 and Its Receptors in Human Tubular Cells

The non-canonical NF-κB pathway in immunity and inflammation

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