scholarly journals A hősokkfehérjék hatása a máj ischaemiás-reperfúziós károsodására

2016 ◽  
Vol 157 (42) ◽  
pp. 1659-1666
Author(s):  
Andrea Rostás ◽  
Ahmed Sabry ◽  
Subhamay Ghosh
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Diseases ◽  
Diagnostic Role ◽  
Hepatic Ischemia Reperfusion ◽  
Shock Proteins

Hepatic ischemia-reperfusion injury as a result of inflow obstruction is a major cause of morbidity and mortality associated with liver pathologies and surgery. Heat shock proteins, a family of stress-inducible proteins involved in maintaining cell homeostasis and regulating the immune system play a major role in liver regeneration. They serve as crucial indicators of ischemia-reperfusion injury in human liver and influence liver function and recovery. The primary objectives of this article are to review the potential role of heat shock proteins as a diagnostic marker for liver diseases and therapeutic target in critical illness. The review will start by focusing on the essentials of heat shock proteins as an endogenous system as it relates to hepatic injury. It will elucidate the influence of heat shock protein-70 on hepatic diseases and ischemia-reperfusion. It will then look at their potential diagnostic role and finally highlights its activities as a possible therapeutic tool. Orv. Hetil., 2016, 157(42), 1659–1666.

Modified Mild Heat Shock Modality Attenuates Hepatic Ischemia/Reperfusion Injury

2010 ◽  
Vol 162 (2) ◽  
pp. 213-220 ◽  
Author(s):  
Mariko Oba ◽  
Mary Ann Suico ◽  
Saori Morino ◽  
Shuichiro Yano ◽  
Takashi Matsuno ◽  
...  
Keyword(s):  
Heat Shock ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Mild Heat ◽  
Hepatic Ischemia Reperfusion

scholarly journals Heat Shock Proteins in Oxidative Stress and Ischemia/Reperfusion Injury and Benefits from Physical Exercises: A Review to the Current Knowledge

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jakub Szyller ◽  
Iwona Bil-Lula
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Physical Exercises ◽  
Shock Proteins

Heat shock proteins (HSPs) are molecular chaperones produced in response to oxidative stress (OS). These proteins are involved in the folding of newly synthesized proteins and refolding of damaged or misfolded proteins. Recent studies have been focused on the regulatory role of HSPs in OS and ischemia/reperfusion injury (I/R) where reactive oxygen species (ROS) play a major role. ROS perform many functions, including cell signaling. Unfortunately, they are also the cause of pathological processes leading to various diseases. Biological pathways such as p38 MAPK, HSP70 and Akt/GSK-3β/eNOS, HSP70, JAK2/STAT3 or PI3K/Akt/HSP70, and HSF1/Nrf2-Keap1 are considered in the relationship between HSP and OS. New pathophysiological mechanisms involving ROS are being discovered and described the protein network of HSP interactions. Understanding of the mechanisms involved, e.g., in I/R, is important to the development of treatment methods. HSPs are multifunctional proteins because they closely interact with the antioxidant and the nitric oxide generation systems, such as HSP70/HSP90/NOS. A deficiency or excess of antioxidants modulates the activation of HSF and subsequent HSP biosynthesis. It is well known that HSPs are involved in the regulation of several redox processes and play an important role in protein-protein interactions. The latest research focuses on determining the role of HSPs in OS, their antioxidant activity, and the possibility of using HSPs in the treatment of I/R consequences. Physical exercises are important in patients with cardiovascular diseases, as they affect the expression of HSPs and the development of OS.

Role of heat shock protein 70 in hepatic ischemia-reperfusion injury in mice

2007 ◽  
Vol 292 (4) ◽  
pp. G1141-G1149 ◽  
Author(s):  
Satoshi Kuboki ◽  
Rebecca Schuster ◽  
John Blanchard ◽  
Timothy A. Pritts ◽  
Hector R. Wong ◽  
...  
Keyword(s):  
Heat Shock ◽  
Liver Injury ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neutrophil Accumulation ◽  
Hepatic Ischemia ◽  
Recombinant Hsp70 ◽  
Hepatic Ischemia Reperfusion

It is well established that liver ischemia-reperfusion induces the expression of heat shock protein (HSP) 70. However, the biological function of HSP70 in this injury is unclear. In this study, we sought to determine the role of HSP70 in hepatic ischemia-reperfusion injury in mice. Male mice were subjected to 90 min of partial hepatic ischemia followed by up to 8 h of reperfusion. HSP70 was rapidly upregulated after reperfusion. To explore the function of HSP70, sodium arsenite (8 mg/kg iv) was injected before surgery. We found that this dose induced HSP70 expression within 6 h of treatment. Induction of HSP70 with arsenite resulted in a >50% reduction in liver injury as determined by serum transaminases and histology. In addition, arsenite similarly reduced liver neutrophil recruitment and liver nuclear factor-κB activation, and attenuated serum levels of tumor necrosis factor-α and macrophage inflammatory protein-2, but increased levels of interleukin (IL)-6. In HSP70 knockout mice, arsenite did not protect against liver injury but did reduce liver neutrophil accumulation. Arsenite-induced reductions in neutrophil accumulation in HSP70 knockout mice were found to be mediated by IL-6. To determine whether extracellular HSP70 contributed to the injury, recombinant HSP70 was injected before surgery. Intravenous injection of 10 μg of recombinant HSP70 had no effect on liver injury after ischemia-reperfusion. The data suggest that intracellular HSP70 is directly hepatoprotective during ischemia-reperfusion injury and that extracellular HSP70 is not a significant contributor to the injury response in this model. Targeted induction of HSP70 may represent a potential therapeutic option for postischemic liver injury.

PRIOR INDUCTION OF HEAT SHOCK PROTEINS BY A NITRIC OXIDE DONOR ATTENUATES CARDIAC ISCHEMIA/REPERFUSION INJURY IN THE RAT1

2000 ◽  
Vol 69 (12) ◽  
pp. 2530-2537 ◽  
Author(s):  
Masamichi Katori ◽  
Tohru Tamaki ◽  
Tsuyoshi Takahashi ◽  
Mitsuko Tanaka ◽  
Akio Kawamura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Nitric Oxide Donor ◽  
Shock Proteins

Differential expression of heat shock proteins 70-1 and 70-2 mRNA after ischemia-reperfusion injury of rat kidney

1999 ◽  
Vol 27 (5) ◽  
pp. 306-311 ◽  
Author(s):  
Ziya Akçetin ◽  
Reinhard Pregla ◽  
Dorothea Darmer ◽  
Hans Heynemann ◽  
Johannes Haerting ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Differential Expression ◽  
Ischemia Reperfusion Injury ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Shock Proteins

HEAT SHOCK PROTEINS (HSPs): BIOMARKERS OF ISCHEMIA/REPERFUSION INJURY?

Shock ◽  
2002 ◽  
Vol 18 (Supplement) ◽  
pp. 9
Author(s):  
M C. Guisasola ◽  
M A. Peñaranda ◽  
L. López-Bescós ◽  
F. Asensio ◽  
A. Suárez ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Shock Proteins
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