p38 MAPK phosphorylation and NF-kappaB activation in human crescentic glomerulonephritis

Sakai, Norihiko; Wada, Takashi; Furuichi, Kengo; Iwata, Yasunori; Yoshimoto, Keiichi; Kitagawa, Kiyoki; Kokubo, Satoshi; Kobayashi, Motoo; Takeda, Shin‐ichi; Kida, Hiroshi; Kobayashi, Kenichi; Mukaida, Naofumi; Matsushima, Kouji; Yokoyama, Hitoshi

doi:10.1093/ndt/17.6.998

Cited by 80 publications

(67 citation statements)

References 27 publications

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“…There was also a correlation between renal failure and the number of p-p38+ glomerular, tubular, and interstitial cells; while proteinuria correlated with the number of p-p38+ podocytes, tubular, and interstitial cells (10,20). A significant increase in p38 activation is also evident in human and experimental diabetic nephropathy (20,21), with the number of p-p38+ tubulointerstitial cells reflecting the severity of tubulointerstitial lesions (22). These studies suggest that p38 activation may play an important pathogenic role in human renal diseases.…”

Section: Sapk In Human Kidney Diseasementioning

confidence: 97%

The role of stress-activated protein kinase signaling in renal pathophysiology

Liu

Nikolic-Paterson

2008

Braz J Med Biol Res

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Two major stress-activated protein kinases are the p38 mitogen-activated protein kinase (MAPK) and the c-Jun amino terminal kinase (JNK). p38 and JNK are widely expressed in different cell types in various tissues and can be activated by a diverse range of stimuli. Signaling through p38 and JNK is critical for embryonic development. In adult kidney, p38 and JNK signaling is evident in a restricted pattern suggesting a normal physiological role. Marked activation of both p38 and JNK pathways occurs in human renal disease, including glomerulonephritis, diabetic nephropathy and acute renal failure. Administration of small molecule inhibitors of p38 and JNK has been shown to provide protection from renal injury in different types of experimental kidney disease through inhibition of renal inflammation, fibrosis, and apoptosis. In particular, a role for JNK signaling has been identified in macrophage activation resulting in up-regulation of pro-inflammatory mediators and the induction of renal injury. The ability to provide renal protection by blocking either p38 or JNK indicates a lack of redundancy for these two signaling pathways despite their activation by common stimuli. Therefore, the stress-activated protein kinases, p38 and JNK, are promising candidates for therapeutic intervention in human renal diseases.

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Section: Sapk In Human Kidney Diseasementioning

confidence: 97%

The role of stress-activated protein kinase signaling in renal pathophysiology

Liu

Nikolic-Paterson

2008

Braz J Med Biol Res

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“…In general, NF-B activates in macrophages and glomerular (including podocytes in proteinuric diseases) and tubular parenchymal cells and correlates with parameters of severity of disease such as proteinuria or inflammation. 59,[61][62][63][64][65] These data have been interpreted as supportive for the role of NF-B in promoting inflammation; however, inflammation itself will promote NF-B activation, and because these data are descriptive, the precise role of the various NF-B complexes in human kidney injury remains uncertain. Functional evidence of NF-B activation has been obtained by transcriptomics-based pathway mapping 66 ; in progressive diabetic nephropathy, there is upregulation of 54 of 138 known NF-B targets with special enrichment in NF-B/IRFF module target genes.…”

Section: Nf-b Activation In Experimental and Human Renal Diseasementioning

confidence: 99%

NF-κB in Renal Inflammation

Sanz¹,

Sanchez-Niño²,

Ramos³

et al. 2010

Journal of the American Society of Nephrology

506

379

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“…NF-B is activated in several forms of experimental and human glomerulonephritis, including immune complex kidney disease (8 -11), crescentic glomerulonephritis (12), and lupus nephritis (9), and it activates iNOS in these settings. A variety of inflammatory stimuli, such as IL-1␤ (13,14), bacterial lipopolysaccharide and IFN-␥ (14), and oxidative stress (15) activate this transcription factor in mesangial cells.…”

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confidence: 99%