2007
DOI: 10.1681/asn.2006060604
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A Pathogenic Role for c-Jun Amino-Terminal Kinase Signaling in Renal Fibrosis and Tubular Cell Apoptosis

Abstract: Renal fibrosis and tubular apoptosis are common mechanisms of progressive kidney disease. In vitro studies have implicated the c-Jun amino-terminal kinase (JNK) pathway in these processes. Both of the major JNK isoforms, JNK1 and JNK2, are expressed in the kidney, but their relative contribution to JNK signaling is unknown. This study investigated the role of JNK signaling in renal fibrosis and tubular apoptosis in the unilateral ureteral obstruction model using two different approaches: (1) Mice that were def… Show more

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Cited by 161 publications
(155 citation statements)
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“…Genetic deletion of either Jnk1 or Jnk2 did not prevent the marked activation of JNK signaling seen in the obstructed kidney, or affect the development of renal fibrosis, demonstrating redundancy between the two JNK isoforms. However, tubular epithelial cell apoptosis was significantly reduced in Jnk1-/-mice, identifying a specific role for this isoform in one aspect of renal injury (19). The identification of both MKK3 and JNK1 in tubular apoptosis in the obstructed kidney is supported by studies in which stretch-induced apoptosis of cultured tubular cells is dependent upon p38 and JNK signaling (44).…”
Section: Sapk In Interstitial Fibrosismentioning
confidence: 97%
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“…Genetic deletion of either Jnk1 or Jnk2 did not prevent the marked activation of JNK signaling seen in the obstructed kidney, or affect the development of renal fibrosis, demonstrating redundancy between the two JNK isoforms. However, tubular epithelial cell apoptosis was significantly reduced in Jnk1-/-mice, identifying a specific role for this isoform in one aspect of renal injury (19). The identification of both MKK3 and JNK1 in tubular apoptosis in the obstructed kidney is supported by studies in which stretch-induced apoptosis of cultured tubular cells is dependent upon p38 and JNK signaling (44).…”
Section: Sapk In Interstitial Fibrosismentioning
confidence: 97%
“…The JNK signaling pathway also shows dramatic activation in tubular epithelial cells and myofibroblasts in the obstructed kidney (19). Administration of a JNK inhibitor was effective in preventing c-Jun phosphorylation and significantly reducing interstitial myofibroblast accumulation and collagen synthesis and deposition.…”
Section: Sapk In Interstitial Fibrosismentioning
confidence: 98%
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“…Angiotensin II promotes ECM synthesis by activating the ERK and p38 pathways (12). ERK, p38 and JNK are also involved in the process of renal fibrosis in UUO rats (13)(14)(15). The activation of ERK and p38 induces the synthesis of TGF-β1 to form a vicious cycle aggravating renal fibrosis (16).…”
Section: Introductionmentioning
confidence: 99%