The role of cycloxygenase-2 in the rodent kidney following ischaemia/reperfusion injury in vivo

2007 ◽  
Vol 562 (1-2) ◽  
pp. 148-154 ◽  
Author(s):  
Nimesh S.A. Patel ◽  
Salvatore Cuzzocrea ◽  
Massimo Collino ◽  
Prabal K. Chaterjee ◽  
Emanuela Mazzon ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

Gene Silencing using siRNA for Preventing Liver Ischaemia-Reperfusion Injury

2018 ◽  
Vol 24 (23) ◽  
pp. 2692-2700 ◽  
Author(s):  
H. Susana Marinho ◽  
Paulo Marcelino ◽  
Helena Soares ◽  
Maria Luísa Corvo
Keyword(s):  
Gene Silencing ◽  
Reperfusion Injury ◽  
Therapeutic Potential ◽  
Major Complication ◽  
Ischaemia Reperfusion Injury ◽  
Small Interference Rna ◽  
Ischaemia Reperfusion ◽  
Promising Therapeutic Approach ◽  
Sirna Therapy

Background: Ischaemia-reperfusion injury (IRI), a major complication occurring during organ transplantation, involves an initial ischemia insult, due to loss of blood supply, followed by an inflammation-mediated reperfusion injury. A variety of molecular targets and pathways involved in liver IRI have been identified. Gene silencing through RNA interference (RNAi) by means of small interference RNA (siRNA) targeting mediators of IRI is a promising therapeutic approach. Objective: This study aims at reviewing the use of siRNAs as therapeutic agents to prevent IRI during liver transplantation. Method: We review the crucial choice of siRNA targets and the advantages and problems of the use of siRNAs. Results: We propose possible targets for siRNA therapy during liver IRI. Moreover, we discuss how drug delivery systems, namely liposomes, may improve siRNA therapy by increasing siRNA stability in vivo and avoiding siRNA off-target effects. Conclusion: siRNA therapeutic potential to preclude liver IRI can be improved by a better knowledge of what molecules to target and by using more efficient delivery strategies.

Role of complement regulatory membrane proteins in ischaemia-reperfusion injury of rat gastric mucosa

1999 ◽  
Vol 14 (10) ◽  
pp. 967-972 ◽  
Author(s):  
Fumihiro Iwata ◽  
Takashi Joh ◽  
Toyohiro Tada ◽  
Noriko Okada ◽  
B Paul Morgan ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Membrane Proteins ◽  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Rat Gastric Mucosa

The role of oxygen free radicals in the ischaemia - reperfusion injury

1987 ◽  
pp. 337-346
Author(s):  
F. Cuccurullo ◽  
A. Mezzetti ◽  
A. Arduini ◽  
E. Porreca ◽  
D. Lapenna ◽  
...  
Keyword(s):  
Free Radicals ◽  
Reperfusion Injury ◽  
Oxygen Free Radicals ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

Linking proximal and downstream signalling events in hepatic ischaemia/reperfusion injury

2006 ◽  
Vol 34 (5) ◽  
pp. 957-959 ◽  
Author(s):  
G. Jeyabalan ◽  
A. Tsung ◽  
T.R. Billiar
Keyword(s):  
Reperfusion Injury ◽  
Immune Surveillance ◽  
High Mobility ◽  
Intracellular Signalling ◽  
Ischaemia Reperfusion Injury ◽  
Signalling Molecules ◽  
Ischaemia Reperfusion ◽  
The Many ◽  
Molecular Patterns

Hepatic I/R (ischaemia/reperfusion) injury occurs in a variety of clinical settings including transplantation, elective liver resections and trauma. One of the challenges in studying the pathophysiology of I/R injury is the fact that the liver plays a central role in a variety of metabolic pathways in addition to governing aspects of immune surveillance and tolerance. The pathways activated in response to insults as varied as toxins, microbial and endogenous ligands and I/R may share common elements. The multiple intracellular signalling cascades involved in this process and the initiating events are still under investigation. Recent work on the role of TLRs (Toll-like receptors) in I/R injury has elucidated some of the more proximal signalling events in the pathway. In addition to the well-established role of signalling molecules such as NO (nitric oxide) in mediating damage or protection following hepatic I/R, more recent studies have focused on the participation of endogenous danger signals or DAMPs (damage-associated molecular patterns) such as HMGB1 (high-mobility group box 1). The complex interplay between HMGB1, TLRs and the many intracellular signalling molecules and pathways is illustrative of how our understanding of hepatic I/R injury is continually evolving.

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