Heme oxygenase system in hepatic ischemia-reperfusion injury

Richards, James; Wigmore, Stephen J.; Devey, Luke

doi:10.3748/wjg.v16.i48.6068

Cited by 29 publications

(24 citation statements)

References 122 publications

(134 reference statements)

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“…Therefore, a potential role for biliverdin and carbon monoxide as inhibitors of viral replication (via their antioxidative effects) requires further study [53] . Recent advances in molecular biology have provided new approaches to reducing hepatic IRI with gene therapy [55] . Liver transplantation [56] (a commonly employed treatment for hepatic failure) is still a limited means of therapy and has many drawbacks, including high monetary costs for the patient and donor shortages [8] .…”

Section: Ho-1 As a Potential Therapeutic Target In Liver Diseasesmentioning

confidence: 99%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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The activation of heme oxygenase-1 (HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and rejection. In addition, the products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis C and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the CO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of REVIEW 541October 27, 2013|Volume 5|Issue 10| WJH|www.wjgnet.com low concentrations of exogenous CO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload (with signs of a chronic hepatitis) and iron deficiency anemia (with paradoxical increased levels of ferritin). Hypoxia induces HO-1 expression in multiple rodent, bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types (endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and CO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury.

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Section: Ho-1 As a Potential Therapeutic Target In Liver Diseasesmentioning

confidence: 99%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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“…Heme oxygenase-1 (HO1), the rate-limiting enzyme in heme degradation with a strong anti-inflammatory and antiapoptotic role, can protect against various injuries, such as ischemic-reperfusion injury [4]. However, the advantages in anti-apoptotic and cytoprotective roles of HO-1 turn out to induce tumor-progression in cancer chemotherapeutic [5].…”

mentioning

confidence: 99%

MiR-200c sensitizes clear-cell renal cell carcinoma cells to sorafenib and imatinib by targeting heme oxygenase-1

Gao¹,

Peng²,

Peng³

2014

neo

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Clear-cell renal cell carcinoma is a highly treatment-resistant tumor type. Heme oxygenase-1 plays an anti-apoptotic role in cancer chemotherapeutic inducing tumor-progression. The miR-200 family was involved in the process of mesenchymal-epithelial transition (MET) during renal development. In the present study, we demonstrated the regulatory relationship between miR-200c and HO-1. We provided evidences to elucidate that miR-200c could sensitize ccRCC cells to sorafenib or imatinib to inhibit cell proliferation, at least partly by targeting HO-1. Moreover, the correlation between miR-200c and HO-1 expression level and drug resistance in ccRCC was also determined. Combined application with chemotherapeutic drugs, miR-200c, a HO-1 inhibitor, may enhance the efficiency of therapy by promoting both apoptosis and autophagy.

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“…Literature data indicate that supplementation with L-arginine has beneficial effect in clinical conditions observed in impaired endothelial function, increased production of oxygen free radicals, increased lipid peroxidation and, consequently, damage to multiple organs [23,26]. Many studies have revealed a positive improvement of endothelial function after administration of L-arginine to smokers, patients with idiopathic mild hypertension, patients with pregnancy-induced hypertension and patients with hypercholesteremia [9,16,18,25].…”

Section: Introductionmentioning

confidence: 99%

“…Free radicals damage can lead to destruction of cell membrane structures. The level of ischemia-reperfusion damage can be assessed by determining the characteristic parameters for a given tissue, which normally occur in the blood serum in small amounts and after damage to cellular structures "leak" into the blood [1,23].…”

Section: Introductionmentioning

confidence: 99%

The influence of short-term l-arginine supplementation on rats’ muscular and hepatic cells in ischemia–reperfusion syndrome

et al. 2011

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Due to the complex mechanisms of L-arginine activity, it is difficult to determine the clinical significance of supplementation with this amino acid. The objective of this study was to determine the influence of short-term supplementation with L-arginine in stress conditions, induced by ischemia-reperfusion syndrome, by assessing the damage to muscular and hepatic cells on the basis of creatine kinase (CK), alanine aminotransferase (ALAT) and aspartic aminotransferase (AspAT) activity in blood and the level of oxygen free radicals in analyzed tissues of rats. We observed that induced ischemia of hind limb caused an increase in CK, ALAT and AspAT activity and an increase in the level of free radicals in liver, but not in skeletal muscle. Supplementation with L-arginine led to a reduction in serum activity of CK and AspAT and reduction of the level of free radicals in analysed tissues. Simultaneous supplementation with L -arginine AND L-NAME resulted in a reversal of changes induced by L-arginine supplementation in the case of AspAT and free radicals in skeletal muscle. The results indicate that under conditions of ischemia-reperfusion, short-term administration of L-arginine has a protective effect on skeletal muscle manifesting itself by reduction of CK in the serum and reduction of free radicals level in THIS tissue.

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Heme oxygenase system in hepatic ischemia-reperfusion injury

Cited by 29 publications

References 122 publications

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

MiR-200c sensitizes clear-cell renal cell carcinoma cells to sorafenib and imatinib by targeting heme oxygenase-1

The influence of short-term l-arginine supplementation on rats’ muscular and hepatic cells in ischemia–reperfusion syndrome

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