The inflammatory response to ischemic acute kidney injury: a result of the ‘right stuff’ in the ‘wrong place’?

Lu, Christopher Y.; Hartono, John; Senitko, Martin; Chen, Jianlin

doi:10.1097/mnh.0b013e3280403c4e

Cited by 47 publications

(50 citation statements)

References 135 publications

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“…RAGE is expressed in a wide range of renal cells and mediates a variety of inflammatory responses in renal diseases [7] , but its role in renal I/R injury was unknown [13] . Therefore, we investigated the contribution of RAGE in renal I/R.…”

Section: Discussionmentioning

confidence: 99%

“…These findings indicate that the role of RAGE in I/R injury is tissue specific. RAGE is a multiligand receptor of the immunoglobulin (Ig) superfamily and is expressed on a wide range of cell types, including renal mesangial cells, (proximal) tubuli, podocytes and Bowman's capsule [3][4][5][6]13] . In line with these results, we showed RAGE expression on podocyte and tubuli but also on cells of the collecting duct.…”

Section: Discussionmentioning

confidence: 99%

“…RAGE mediates a variety of inflammatory responses in renal diseases but its role in renal I/R injury has not been investigated yet [7,13] . We subjected WT and RAGE KO mice to renal I/R and sacrificed them at different time-points.…”

Section: Rage Deficiency Does Not Lead To Impaired Renal Function Aftmentioning

confidence: 99%

“…The receptor for advanced glycation end products (RAGE) is a multiligand PRR that is expressed in all tissues and on a wide range of cell types, including renal mesangial cells, (proximal) tubuli, podocytes and Bowman's capsule [2][3][4][5][6] and mediates a variety of inflammatory responses in renal diseases [7] . RAGE blockade or deficiency has been shown to suppress hepatic, cardiac, lung and brain I/R-induced injury [8][9][10][11][12] ; however, the contribution of RAGE in renal I/R-induced injury is unknown [13] . Therefore, in the current study we investigated the contribution of RAGE in renal I/R-induced injury.…”

mentioning

confidence: 99%

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RAGE Does Not Contribute to Renal Injury and Damage upon Ischemia/Reperfusion-Induced Injury

Dessing¹,

Pulskens²,

Teske³

et al. 2011

J Innate Immun

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Rage Deficiency Does Not Lead To Impaired Renal Function Aftmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

RAGE Does Not Contribute to Renal Injury and Damage upon Ischemia/Reperfusion-Induced Injury

Dessing¹,

Pulskens²,

Teske³

et al. 2011

J Innate Immun

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“…24,59 Release of HMGB1 has been reported after IRI. 58,[60][61][62] Data from Lu et al 63 and our findings 25 demonstrate that the ischemic kidney is the originator of surging HMGB1 in the circulation, that endothelial cells contribute to it, and that uric acid signaling can mimic this process both in vitro and in vivo. We showed that after ischemic insult, HMGB1 is released into the renal circulation within 1-3 hours (Figure 1, B and C).…”

Section: Systemic Inflammation: Three Waves Of Danger Signalingmentioning

confidence: 99%

Messengers without Borders

Ratliff

Rabadi

Vasko

et al. 2013

Journal of the American Society of Nephrology

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The list of signals sent by an injured organ to systemic circulation, so-called danger signals, is growing to include multiple metabolites and secreted moieties, thus revealing a highly complex and integrated network of interlinked systemic proinflammatory and proregenerative messages. Emerging new data indicate that, apart from the well established local inflammatory response to AKI, danger signaling unleashes a cascade of precisely timed, interdependent, and intensity-gradated mediators responsible for development of the systemic inflammatory response. This fledgling realization of the importance of the systemic inflammatory response to the localized injury and inflammation is at the core of this brief overview. It has a potential to explain the additive effects of concomitant diseases or preexisting chronic conditions that can prime the systemic inflammatory response and exacerbate it out of proportion to the actual degree of acute kidney damage. Although therapies for ameliorating AKI per se remain limited, a potentially powerful strategy that could reap significant benefits in the future is to modulate the intensity of danger signals and consequently the systemic inflammatory response, while preserving its intrinsic proregenerative stimuli.

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Annexin 1 mimetic peptide protects against renal ischemia/reperfusion injury in rats

et al. 2010

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Inflammation is currently recognized as a key mechanism in the pathogenesis of renal ischemia-reperfusion (I/R) injury. The importance of infiltrating neutrophil, lymphocytes, and macrophage in this kind of injury has been assessed with conflicting results. Annexin 1 is a protein with potent neutrophil anti-migratory activity. In order to evaluate the effects of annexin A1 on renal I/R injury, uninephrectomized rats received annexin A1 mimetic peptide Ac2-26 (100 μg) or vehicle before 30 min of renal artery clamping and were compared to sham surgery animals. Annexin A1 mimetic peptide granted a remarkable protection against I/R injury, preventing glomerular filtration rate and urinary osmolality decreases and acute tubular necrosis development. Annexin A1 infusion aborted neutrophil extravasation and attenuated macrophage infiltration but did not prevent tissue lymphocyte traffic. I/R increased annexin A1 expression (assessed by transmission electron microscopy) in renal epithelial cells, which was attenuated by exogenous annexin A1 infusion. Additionally, annexin A1 reduced I/R injury in isolated proximal tubules suspension. Annexin A1 protein afforded striking functional and structural protection against renal I/R. These results point to an important role of annexin A1 in the epithelial cells defense against I/R injury and indicate that neutrophils are key mediators for the development of tissue injury after renal I/R. If these results were confirmed in clinical studies, annexin A1 might emerge as an important tool to protect against I/R injury in renal transplantation and in vascular surgery.

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The inflammatory response to ischemic acute kidney injury: a result of the ‘right stuff’ in the ‘wrong place’?

Abstract: The concepts discussed in this review are important for clinical medicine. Drugs and genetic manipulation may ameliorate ischemic kidney injury by regulating the inflammatory response to cell injury.

Cited by 47 publications

References 135 publications

RAGE Does Not Contribute to Renal Injury and Damage upon Ischemia/Reperfusion-Induced Injury

RAGE Does Not Contribute to Renal Injury and Damage upon Ischemia/Reperfusion-Induced Injury

Messengers without Borders

Annexin 1 mimetic peptide protects against renal ischemia/reperfusion injury in rats

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