Heat Shock Preconditioning on Mitochondria during Warm Ischemia in Rat Livers

Ishikawa, Yukihiro; Yamamoto, Yūzō; Kume, Makoto; Yamagami, Kazuhiko; Yamamoto, Hidekazu; Kimoto, Sayuri; Sakai, Yoshiharu; Yamamoto, Masayuki; Yamaoka, Yoshio

doi:10.1006/jsre.1999.5770

Cited by 23 publications

(13 citation statements)

References 49 publications

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“…Ischemia causes consumption of energy-rich phosphates [24] and loss of integrity of mitochondrial membranes [25]. This mitochondrial dysfunction results in reduced regeneration of mitochondrial energetics also during subsequent reperfusion [26].…”

Section: Discussionmentioning

confidence: 99%

Improvement of nutritive perfusion after free tissue transfer by local heat shock-priming-induced preservation of capillary flowmotion

Rücker¹,

Kadirogullari²,

Vollmar³

et al. 2005

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Improvement of nutritive perfusion after free tissue transfer by local heat shock-priming-induced preservation of capillary flowmotion

Rücker¹,

Kadirogullari²,

Vollmar³

et al. 2005

Journal of Surgical Research

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“…In the rat liver, tolerance to ischemic injury has been associated with production of various inducible HSPs: HSP72 [30, 94], HSP73 [30]and HSP70 and HO-1/HSP32 [95, 96]. Ishikawa et al [61]have proposed that in heat shock-preconditioned rat livers HSPs maintain mitochondrial membrane integrity during the ischemic episode, to produce energy-rich phosphates during reperfusion and thus contribute to ischemic tolerance. In an in vivo study in rats by Kume et al [29]the reduced postischemic hepatocellular injury and improved survival was associated with overexpression of HSP72 in ischemically preconditioned livers as well as in the livers preconditioned with heat shock.…”

Section: Possible Mechanisms Of Preconditioningmentioning

confidence: 99%

“…Molecules released during ischemia attach to cellular receptors and contribute to preconditioning response. The candidate compounds implicated in liver IPC include adenosine [17, 20, 25, 48, 49], protein kinase C (PKC) [53, 54, 55], nitric oxide (NO) [13, 17, 20, 26, 41, 42], heat shock proteins (HSPs) [29, 61], tyrosine kinases [52], mitogen-activated protein kinases [55], oxidative stress [35, 50], nuclear factor ĸB (NF-ĸB) [62, 63], and modulation of apoptosis cascade [14, 27]. However the characterizations of these candidate compounds into different processes in the preconditioning cascade such as initiating trigger, signalling pathway and end effector are not defined and the interrelationship between these processes is unknown.…”

Section: Possible Mechanisms Of Preconditioningmentioning

confidence: 99%

Protection of the Liver by Ischemic Preconditioning: A Review of Mechanisms and Clinical Applications

Koti¹,

Seifalian²,

Davidson³

2003

Dig Surg

115

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Ischemic preconditioning refers to the endogenous mechanism of protection against a sustained ischemic insult following an initial, brief ischemic stimulus. Ischemia-reperfusion injury of the liver is a major cause of morbidity and mortality in liver surgery and transplantation and ischemic preconditioning is a promising strategy for improving the outcome of liver surgery. The preconditioning phenomenon was first described in a canine model of myocardial ischemia-reperfusion injury in 1986 and since then has been shown to exist in other organs including skeletal muscle, brain, kidneys, retina and liver. In the liver, the preconditioning effect has been demonstrated in rodents and a recent study has demonstrated human clinical benefits of preconditioning during hemihepatectomies. Ischemic preconditioning has been described as an adaptive response and although the precise mechanism of hepatoprotection from preconditioning is unknown it is likely to be a receptor-mediated process. Several hypotheses have been proposed and this review assesses possible mechanisms of ischemic preconditioning and its role in hepatic surgery and liver transplantation. The future lies in defining the mechanisms of the ischemic preconditioning effect to allow drug targeting to induce the preconditioning response.

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“…The underlying mechanism is thought to rely on the modification of gene expression resulting in protein production as its effectors [110] . Various substances have been implicated as key effectors in liver IPC including adenosine [111][112][113][114] , protein kinase C [115][116][117] , NO [118][119][120][121] , heatshock proteins [122,123] , tyrosine kinases [124] , MAPKs [117] , oxidative stress [125,126] and NF-κB [127,128] . The beneficial effects of IPC on the liver following IRI include decrease in severity of liver necrosis [129] , antiapoptotic effects [130] , preservation of liver microcirculation [131,132] and improvement in survival rate [119] , and more recently, its role in liver regeneration is currently being evaluated.…”

Section: Ischaemic Preconditioning In Liver Regenerationmentioning

confidence: 99%

Role of ischaemic preconditioning in liver regeneration following major liver resection and transplantation

Gomez¹

2007

WJG

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Liver ischaemic preconditioning (IPC) is known to protect the liver from the detrimental effects of ischaemicreperfusion injury (IRI), which contributes significantly to the morbidity and mortality following major liver surgery. Recent studies have focused on the role of IPC in liver regeneration, the precise mechanism of which are not completely understood. This review discusses the current understanding of the mechanism of liver regeneration and the role of IPC in this setting. Relevant articles were reviewed from the published literature using the Medline database. The search was performed using the keywords "liver", "ischaemic reperfusion", "ischaemic preconditioning", "regeneration", "hepatectomy" and "transplantation". The underlying mechanism of liver regeneration is a complex process involving the interaction of cytokines, growth factors and the metabolic demand of the liver. IPC, through various mediators, promotes liver regeneration by up-regulating growthpromoting factors and suppresses growth-inhibiting factors as well as damaging stresses. The increased understanding of the cellular mechanisms involved in IPC will enable the development of alternative treatment modalities aimed at promoting liver regeneration following major liver resection and transplantation.

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Heat Shock Preconditioning on Mitochondria during Warm Ischemia in Rat Livers

Abstract: Heat shock preconditioning of the liver protected mitochondria from loss of membrane integrity during ischemia and contributed to their ability to produce energy-rich phosphates during reperfusion.

Cited by 23 publications

References 49 publications

Improvement of nutritive perfusion after free tissue transfer by local heat shock-priming-induced preservation of capillary flowmotion

Improvement of nutritive perfusion after free tissue transfer by local heat shock-priming-induced preservation of capillary flowmotion

Protection of the Liver by Ischemic Preconditioning: A Review of Mechanisms and Clinical Applications

Role of ischaemic preconditioning in liver regeneration following major liver resection and transplantation

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