SP600125, a selective JNK inhibitor, protects ischemic renal injury via suppressing the extrinsic pathways of apoptosis

Yan, Wei; Ji, Huai-Xue; Xing, Shu Guo; Pei, Dong‐Sheng; Guan, Qiu-Hua

doi:10.1016/j.lfs.2007.03.010

Cited by 56 publications

(33 citation statements)

References 34 publications

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“…In experimental models of renal injury MAPK inhibitors have shown beneficial effects. Treatment with JNK inhibitors reduced renal damage, collagen accumulation and apoptosis in the models of ureteral obstruction and ischemia reperfusion (35)(36)(37). Similar data were found in obstructed kidneys of JNK1 and JNK2 deficient mice (38).…”

Section: Discussionsupporting

confidence: 65%

Pharmacological Modulation of Epithelial Mesenchymal Transition Caused by Angiotensin II. Role of ROCK and MAPK Pathways

et al. 2008

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Section: Discussionsupporting

confidence: 65%

Pharmacological Modulation of Epithelial Mesenchymal Transition Caused by Angiotensin II. Role of ROCK and MAPK Pathways

et al. 2008

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“…30 Furthermore, JNK blockade prevents tubular damage following renal ischemia/ reperfusion injury. 48 Thus, JNK blockade may exert a direct effect to reduce the degree of tubulointerstitial damage in rat anti-GBM glomerulonephritis.…”

Section: Discussionmentioning

confidence: 98%

Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat

Frank

Flanc

Tesch

et al. 2009

Laboratory Investigation

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“…Moreover, in unilateral ureteral obstruction, JNK inhibition reduced tubulo-interstitial fibrosis (Ma et al, 2007). In addition, JNK inhibition reduces apoptosis of tubular epithelial cells in I/R and in unilateral ureteral obstruction (Ma et al, 2007;Wang et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

c-Jun NH₂-Terminal Kinase Is Crucially Involved in Renal Tubulo-Interstitial Inflammation

Borst

Prakash

Sandovici

et al. 2009

J Pharmacol Exp Ther

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Chronic inflammation is a major outcome determinant in several renal disorders. Induction of monocyte chemoattractant protein (MCP)-1 expression in tubular epithelial cells contributes importantly to the recruitment of inflammatory cells from the circulation toward the damaged tubulo-interstitium. Because the MCP-1 gene contains several c-Jun binding sites, we hypothesized that the c-Jun NH 2 -terminal kinase (JNK) pathway regulates MCP-1 expression and subsequently tubulointerstitial inflammation. This was investigated in cultured rat tubular epithelial cells (NRK-52E) and in the rat unilateral ischemia/reperfusion (I/R) model. In NRK-52E cells, the JNK inhibitor anthra(1,9-cd)pyrazol-6(2H)-one-1,9-pyrazoloanthrone (SP600125) reduced interleukin-1␤-, transforming growth factor-␤-, or bovine serum albumin-induced MCP-1

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SP600125, a selective JNK inhibitor, protects ischemic renal injury via suppressing the extrinsic pathways of apoptosis

Cited by 56 publications

References 34 publications

Pharmacological Modulation of Epithelial Mesenchymal Transition Caused by Angiotensin II. Role of ROCK and MAPK Pathways

Pharmacological Modulation of Epithelial Mesenchymal Transition Caused by Angiotensin II. Role of ROCK and MAPK Pathways

Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat

c-Jun NH₂-Terminal Kinase Is Crucially Involved in Renal Tubulo-Interstitial Inflammation

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SP600125, a selective JNK inhibitor, protects ischemic renal injury via suppressing the extrinsic pathways of apoptosis

Cited by 56 publications

References 34 publications

Pharmacological Modulation of Epithelial Mesenchymal Transition Caused by Angiotensin II. Role of ROCK and MAPK Pathways

Pharmacological Modulation of Epithelial Mesenchymal Transition Caused by Angiotensin II. Role of ROCK and MAPK Pathways

Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat

c-Jun NH2-Terminal Kinase Is Crucially Involved in Renal Tubulo-Interstitial Inflammation

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c-Jun NH₂-Terminal Kinase Is Crucially Involved in Renal Tubulo-Interstitial Inflammation