Ischemic Postconditioning Protects Liver From Ischemia-Reperfusion Injury by Modulating Mitochondrial Permeability Transition

Li, Tsai-Kun; Lee, Tsai-Kun; Tsai, Chung-En; Lai, I-Rue; Lu, Kuo-Shyan

doi:10.1097/tp.0b013e31823ef335

Cited by 32 publications

(30 citation statements)

References 26 publications

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“…53 Opening of the mitochondrial permeability transition pore in liver cells was inhibited by delayed ischaemic postconditioning. 49 It is possible that the reduction in mitochondrial swelling may be due to a lowering of cytosolic Ca 2þ concentrations and inhibition of the opening of mitochondrial permeability transition pore.…”

Section: Discussionmentioning

confidence: 99%

“…48 In contrast, the present study found that ischaemic postconditioning significantly attenuated mitochondria swelling induced by lethal ischaemia and reperfusion. Mitochondrial swelling is related to the opening of the mitochondrial permeability transition pore, 49 with calcium ion (Ca 2þ ) concentration being proportional to the extent of pore opening. 50,51 Overload of Ca 2þ is a pathological characteristic of ischaemia/reperfusion.…”

Section: Discussionmentioning

confidence: 99%

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Role of mitochondrial function in the protective effects of ischaemic postconditioning on ischaemia/reperfusion cerebral damage

Liang

Zhang

et al. 2013

J Int Med Res

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Objective: To investigate the effects of ischaemic postconditioning on brain injury and mitochondria in focal ischaemia and reperfusion, in rats. Methods: Adult male Wistar rats (n ¼ 15 per group) underwent sham surgery, ischaemia (2-h middle cerebral artery occlusion), or ischaemia followed by ischaemic postconditioning (three cycles of 30 s reperfusion/30 s reocclusion). Brain infarction size, neurological function, mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential and mitochondrial swelling were evaluated 24 h postsurgery. Results: Infarct size was significantly smaller, and neurological function was significantly better, in the ischaemic postconditioning group than in the ischaemia group. Ischaemia resulted in significant increases in mitochondrial ROS production and swelling, and a reduction in mitochondrial membrane potential, all of which were significantly reversed by postconditioning. Conclusions: The protective role of ischaemic postconditioning in focal ischaemia/reperfusion may be due to decreased mitochondrial ROS production, reduced mitochondrial membrane potential and suppressed mitochondria swelling. Mitochondria are potential targets for new therapies to prevent brain damage caused by ischaemia and reperfusion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Role of mitochondrial function in the protective effects of ischaemic postconditioning on ischaemia/reperfusion cerebral damage

Liang

Zhang

et al. 2013

J Int Med Res

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“…Although the mechanisms responsible for ischemic PostC of the liver are not fully understood, some studies have shown that the two processes have many similarities [6][7][8]. Recent studies have demonstrated that some agents, such as adenosine A2A receptor agonist [8], rhEPO [9], and sevoflurane [10], can be used as pharmacological inducers of PostC as well as PreC.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, recent studies have proved that several brief cycles of ischemia and reperfusion at the onset of sustained reperfusion after ischemia, termed ischemic postconditioning (PostC), provided protective effects against hepatic IR injury [5][6][7]. PostC is more likely than PreC to be feasible for clinical application because the onset of reperfusion is more predictable.…”

Section: Introductionmentioning

confidence: 99%

“…Although the mechanisms responsible for ischemic PostC of the liver are not as well characterized as those responsible for PreC, recent studies have shown that the two processes have many similarities, including adenosine- [8], phosphoinositide 3-kinase (PI3K)/Akt- [6], and endothelial and inducible nitric oxide synthase (eNOS and iNOS)-mediated NO production [5], as well as inhibition of the opening of the mitochondrial permeability transition pore (mPTP) [7].…”

Section: Introductionmentioning

confidence: 99%

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Milrinone-induced postconditioning reduces hepatic ischemia-reperfusion injury in rats: the roles of phosphatidylinositol 3-kinase and nitric oxide

Toyoda

Tosaka

et al. 2014

Journal of Surgical Research

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Cyclophilin D as a potential therapeutic target of liver ischemia/reperfusion injury by mediating crosstalk between apoptosis and autophagy

Yang

Wang

Xie³

et al. 2023

Chronic Diseases and Translational Medicine

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BackgroundLiver ischemia/reperfusion (I/R) injury is a complex and multifactorial pathophysiological process. It is well recognized that the membrane permeability transition pore (mPTP) opening of mitochondria plays a crucial role in cell death after I/R injury. Cyclophilin D (CypD) is a critical positive regulator of mPTP. However, the effect of CypD on the pathogenesis of liver I/R injury and whether CypD is a potential therapeutic target are still unclear.MethodsWe constructed liver‐specific CypD knockout and AAV8‐peptidyl prolyl isomerase F (PPIF) overexpression mice. Then, a 70% liver I/R injury model was established in mice, with 90 min of ischemia and 6 h of reperfusion. The liver function was detected by the level of serum glutamic pyruvic transaminase (alanine transaminase) and glutamic oxaloacetic transaminase (aspartate aminotransferase), the liver damage score and degree of necrosis were measured by hematoxylin and eosin (H&E) staining of liver tissues. Reactive oxygen species (ROS) staining, apoptosis, and autophagy‐related molecules were used to detect apoptosis and autophagy during liver I/R.ResultsThe liver‐specific knockout of CypD alleviated necrosis and dysfunction in liver I/R injury, by reducing the excessive production of ROS, and inhibiting cell apoptosis and autophagy. On the contrary, overexpression of CypD exacerbated I/R‐induced liver damage.ConclusionWe found that the downregulation of CypD expression alleviated liver I/R injury by reducing apoptosis and autophagy through caspase‐3/Beclin1 crosstalk; in contrast, the upregulation of CypD expression aggravated liver I/R injury. Therefore, interfering with the expression of CypD seems to be a promising treatment for liver I/R injury.

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Ischemic Postconditioning Protects Liver From Ischemia-Reperfusion Injury by Modulating Mitochondrial Permeability Transition

Abstract: iPoC attenuated cell deaths after I/R injury of liver. The protective effects were negated by the addition of ATR--a mPTP opener--and mimicked by injection of NIM811--a mPTP opening inhibitor. The study indicated iPoC conferred protection by modulating mPTP.

Cited by 32 publications

References 26 publications

Role of mitochondrial function in the protective effects of ischaemic postconditioning on ischaemia/reperfusion cerebral damage

Role of mitochondrial function in the protective effects of ischaemic postconditioning on ischaemia/reperfusion cerebral damage

Milrinone-induced postconditioning reduces hepatic ischemia-reperfusion injury in rats: the roles of phosphatidylinositol 3-kinase and nitric oxide

Cyclophilin D as a potential therapeutic target of liver ischemia/reperfusion injury by mediating crosstalk between apoptosis and autophagy

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