scholarly journals Mitogen Activated Protein Kinases in Steatotic and Non-Steatotic Livers Submitted to Ischemia-Reperfusion

2019 ◽  
Vol 20 (7) ◽  
pp. 1785 ◽  
Author(s):  
Jiménez-Castro ◽  
Cornide-Petronio ◽  
Gracia-Sancho ◽  
Casillas-Ramírez ◽  
Peralta
Keyword(s):  
Risk Factor ◽  
Clinical Practice ◽  
Protein Kinases ◽  
Hepatic Steatosis ◽  
Ischemic Preconditioning ◽  
Liver Surgery ◽  
Clinical Studies ◽  
Ischemia Reperfusion ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

: We analyzed the participation of mitogen-activated protein kinases (MAPKs), namely p38, JNK and ERK 1/2 in steatotic and non-steatotic livers undergoing ischemia-reperfusion (I-R), an unresolved problem in clinical practice. Hepatic steatosis is a major risk factor in liver surgery because these types of liver tolerate poorly to I-R injury. Also, a further increase in the prevalence of steatosis in liver surgery is to be expected. The possible therapies based on MAPK regulation aimed at reducing hepatic I-R injury will be discussed. Moreover, we reviewed the relevance of MAPK in ischemic preconditioning (PC) and evaluated whether MAPK regulators could mimic its benefits. Clinical studies indicated that this surgical strategy could be appropriate for liver surgery in both steatotic and non-steatotic livers undergoing I-R. The data presented herein suggest that further investigations are required to elucidate more extensively the mechanisms by which these kinases work in hepatic I-R. Also, further researchers based in the development of drugs that regulate MAPKs selectively are required before such approaches can be translated into clinical liver surgery.

Lipid Peroxidation Activates Mitogen-Activated Protein Kinases in Testicular Ischemia-Reperfusion Injury

2006 ◽  
Vol 176 (4) ◽  
pp. 1666-1672 ◽  
Author(s):  
Pietro Antonuccio ◽  
Letteria Minutoli ◽  
Carmelo Romeo ◽  
Piero Antonio Nicòtina ◽  
Alessandra Bitto ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Reperfusion Injury ◽  
Protein Kinases ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
Testicular Ischemia

scholarly journals Impact of Ischemic Preconditioning on Outcome in Clinical Liver Surgery: A Systematic Review

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Michael J. J. Chu ◽  
Ryash Vather ◽  
Anthony J. R. Hickey ◽  
Anthony R. J. Phillips ◽  
Adam S. J. R. Bartlett
Keyword(s):  
Systematic Review ◽  
Liver Transplantation ◽  
Liver Resection ◽  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Liver Surgery ◽  
Clinical Studies ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatocellular Damage

Background. Ischemia-reperfusion injury is a major cause of post-liver-surgery complications. Ischemic preconditioning (IPC) has been demonstrated to protect against ischemia-reperfusion injury. Clinical studies have examined IPC in liver surgery but with conflicting results. This systematic review aimed to evaluate the effects of IPC on outcome in clinical liver surgery.Methods. An electronic search of OVID Medline and Embase databases was performed to identify studies that reported outcomes in patients undergoing liver surgery subjected to IPC. Basic descriptive statistics were used to summarise data from individual clinical studies.Results. 1093 articles were identified, of which 24 met the inclusion criteria. Seven topics were selected and analysed by subgroup. There were 10 studies in cadaveric liver transplantation, 2 in living-related liver transplantation, and 12 in liver resection. IPC decreases hepatocellular damage in liver surgery as determined by transaminases but does not translate to any significant clinical benefit in orthotopic liver transplant or liver resection.Conclusions. Available clinical evidence does not support routine use of IPC in liver surgery as it does not offer any apparent benefit in perioperative outcome. Further clinical studies will need to be carried out to determine the subset of patients that will benefit from IPC.

scholarly journals The effect of chronic doxorubicin treatment on mitogen-activated protein kinases and heat stress proteins in rat hearts

2008 ◽  
pp. S97-S102
Author(s):  
P Šimončíková ◽  
T Ravingerová ◽  
M Barančík
Keyword(s):  
Heat Stress ◽  
Protein Kinases ◽  
Stress Proteins ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Tissue Samples ◽  
Mitogen Activated Protein Kinases ◽  
Rat Hearts ◽  
Mitogen Activated Protein ◽  
Heat Stress Proteins

The study has been designed to characterize protein systems involved in the responses of rat hearts to chronic doxorubicin (DOX) treatment. We investigated the influence of DOX on cardiac function, mitogen-activated protein kinases (MAPKs) and heat stress proteins (HSPs). Doxorubicin was administered to rats by intraperitoneal injections over a period of 6 weeks. In control and DOX-treated hearts exposed to 20 min global ischemia and 40 min reperfusion the recovery of contractile function after ischemia/reperfusion (I/R) was determined. The levels and phosphorylation state of proteins in tissue samples were analyzed using specific antibodies. We found an activation of extracellular signal-regulated kinases (ERKs) in rat hearts exposed to DOX treatment and better recovery of contractile function after I/R. Analysis of HSPs showed that DOX induced up-regulation of the levels of HSP60 and down-regulation of HSP70 levels. The levels and/or specific phosphorylation of other studied proteins (p38-MAPK, HSP27, HSP90) were not influenced by DOX. The results point to the possible role of ERKs and some HSPs in mechanisms underlying the response of rat hearts to chronic DOX treatment.

scholarly journals Heat Shock Proteins and Mitogen-activated Protein Kinases in Steatotic Livers Undergoing Ischemia-Reperfusion: Some Answers

2006 ◽  
Vol 168 (5) ◽  
pp. 1474-1485 ◽  
Author(s):  
Marta Massip-Salcedo ◽  
Araní Casillas-Ramirez ◽  
Rosah Franco-Gou ◽  
Ramón Bartrons ◽  
Ismail Ben Mosbah ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Protein Kinases ◽  
Ischemia Reperfusion ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
Shock Proteins

Differential Activation of Mitogen-activated Protein Kinases in Ischemic and Anesthetic Preconditioning

2004 ◽  
Vol 100 (1) ◽  
pp. 59-69 ◽  
Author(s):  
Rafaela da Silva ◽  
Thomas Grampp ◽  
Thomas Pasch ◽  
Marcus C. Schaub ◽  
Michael Zaugg
Keyword(s):  
Protein Kinases ◽  
P38 Mapk ◽  
Functional Recovery ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Mitogen Activated Protein Kinases ◽  
Mapk Activity ◽  
Anesthetic Preconditioning ◽  
Mitogen Activated Protein

Background Accumulating evidence pinpoints to the pivotal role of mitogen-activated protein kinases (MAPKs) in the signal transduction underlying cardiac preconditioning. Methods PD98059, an inhibitor of extracellular signal-regulated protein kinase (MEK-ERK1/2), and SB203580, an inhibitor of p38 MAPK, were used to evaluate the role of MAPKs with respect to postischemic functional recovery in isolated perfused rat hearts subjected to ischemic preconditioning (IPC) and anesthetic preconditioning (APC). Western blot analyses were used to determine the degree of ERK1/2 and p38 MAPK activation after the application of the preconditioning stimulus and after ischemia-reperfusion. Immunohistochemical staining served to visualize subcellular localization of activated MAPKs. Results PD98059 and SB203580 abolished postischemic functional recovery in IPC but not in APC. IPC but not APC markedly activated ERK1/2 and p38 MAPK, which were abrogated by coadministration of the specific blockers. Conversely, IPC and APC enhanced ERK1/2 activity after ischemia-reperfusion as compared to nonpreconditioned hearts, and IPC in addition enhanced p38 MAPK activity. Coadministration of PD98059 and SB203580 during IPC but not during APC inhibited postischemically enhanced MAPK activities. Moreover, chelerythrine and 5-hydroxydecanoate, effective blockers of IPC and APC, annihilated IPC- and APC-induced enhanced postischemic responses of MAPKs. Finally, administration of PD98059 during ischemia-reperfusion diminished the protective effects of IPC and APC. Immunohistochemistry revealed increased ERK1/2 activity primarily in intercalated discs and nuclei and increased p38 MAPK activity in the sarcolemma and nuclei of IPC-treated hearts. Conclusions Although MAPKs may orchestrate cardioprotection as triggers and mediators in IPC, they are devoid of triggering, but they may have mediator effects in APC.

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