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Article: Therapeutic potential of heme oxygenase-1/carbon monoxide system against ischemia-reperfusion injury
Title | Therapeutic potential of heme oxygenase-1/carbon monoxide system against ischemia-reperfusion injury |
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Authors | |
Keywords | Anti-apoptotic Anti-inflammatory Anti-oxidative Hemo oxygenase-1/carbon monoxide Ischemia-reperfusion injury Pharmacological induction |
Issue Date | 2017 |
Publisher | Bentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cpd/index.htm |
Citation | Current Pharmaceutical Design, 2017, v. 23 n. 26, p. 3884-3898 How to Cite? |
Abstract | Background: Ischemia-reperfusion (I/R) injury causes the dysfunctions of different major organs, leading to morbidity and mortality on the global scale. Among a battery of therapeutic targets, the heme oxygenase-1 (HO-1)/carbon monoxide (CO) system has been evaluated for the development of new therapies against I/R injury. The enzyme HO-1 catalyzes the degradation of heme into three biologically active end products, namely biliverdin/bilirubin, CO and ferrous ion. Interestingly, CO is one of a few bioactive gaseous molecules with the capability of regulating inflammation, cell survival and growth. In fact, several CO-releasing compounds have been developed for directly reprogramming the intracellular apoptotic, inflammatory and proliferative signaling networks. In parallel, chemical and genetic approaches have also been evaluated for up-regulating HO-1 expression as an endogenous mechanism to ameliorate I/R injury and heal wounds. Methods: In this review, we discussed the recent studies on the therapeutic potential of HO-1/CO system in the treatment of I/R injury in the heart, brain, liver, kidney, lung, intestine and retina. We focused on the activities and underlying mechanisms of various therapeutic strategies to regulate HO-1/CO system against I/R injury. Results: A large number of studies have demonstrated that HO-1/CO system exhibits potent anti-oxidative, antiapoptotic, anti-inflammatory and cytoprotective activities against I/R injury. The regulation of HO-1/CO expression has been achieved either by genetic overexpression of HO-1 cDNA or pharmacological induction with drugs including curcumin and resveratrol. Conclusion: The HO-1/CO system is a potential target for treating I/R injury. Further studies should be directed to in vivo efficacy and clinical application of HO-1/CO system in the therapy of I/R injury. © 2017 Bentham Science Publishers. |
Persistent Identifier | http://hdl.handle.net/10722/241042 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 0.586 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Cheng, Y | - |
dc.contributor.author | Rong, J | - |
dc.date.accessioned | 2017-05-22T09:21:36Z | - |
dc.date.available | 2017-05-22T09:21:36Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | Current Pharmaceutical Design, 2017, v. 23 n. 26, p. 3884-3898 | - |
dc.identifier.issn | 1381-6128 | - |
dc.identifier.uri | http://hdl.handle.net/10722/241042 | - |
dc.description.abstract | Background: Ischemia-reperfusion (I/R) injury causes the dysfunctions of different major organs, leading to morbidity and mortality on the global scale. Among a battery of therapeutic targets, the heme oxygenase-1 (HO-1)/carbon monoxide (CO) system has been evaluated for the development of new therapies against I/R injury. The enzyme HO-1 catalyzes the degradation of heme into three biologically active end products, namely biliverdin/bilirubin, CO and ferrous ion. Interestingly, CO is one of a few bioactive gaseous molecules with the capability of regulating inflammation, cell survival and growth. In fact, several CO-releasing compounds have been developed for directly reprogramming the intracellular apoptotic, inflammatory and proliferative signaling networks. In parallel, chemical and genetic approaches have also been evaluated for up-regulating HO-1 expression as an endogenous mechanism to ameliorate I/R injury and heal wounds. Methods: In this review, we discussed the recent studies on the therapeutic potential of HO-1/CO system in the treatment of I/R injury in the heart, brain, liver, kidney, lung, intestine and retina. We focused on the activities and underlying mechanisms of various therapeutic strategies to regulate HO-1/CO system against I/R injury. Results: A large number of studies have demonstrated that HO-1/CO system exhibits potent anti-oxidative, antiapoptotic, anti-inflammatory and cytoprotective activities against I/R injury. The regulation of HO-1/CO expression has been achieved either by genetic overexpression of HO-1 cDNA or pharmacological induction with drugs including curcumin and resveratrol. Conclusion: The HO-1/CO system is a potential target for treating I/R injury. Further studies should be directed to in vivo efficacy and clinical application of HO-1/CO system in the therapy of I/R injury. © 2017 Bentham Science Publishers. | - |
dc.language | eng | - |
dc.publisher | Bentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cpd/index.htm | - |
dc.relation.ispartof | Current Pharmaceutical Design | - |
dc.subject | Anti-apoptotic | - |
dc.subject | Anti-inflammatory | - |
dc.subject | Anti-oxidative | - |
dc.subject | Hemo oxygenase-1/carbon monoxide | - |
dc.subject | Ischemia-reperfusion injury | - |
dc.subject | Pharmacological induction | - |
dc.title | Therapeutic potential of heme oxygenase-1/carbon monoxide system against ischemia-reperfusion injury | - |
dc.type | Article | - |
dc.identifier.email | Rong, J: jrong@hku.hk | - |
dc.identifier.authority | Rong, J=rp00515 | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.2174/1381612823666170413122439 | - |
dc.identifier.scopus | eid_2-s2.0-85033365974 | - |
dc.identifier.hkuros | 272097 | - |
dc.identifier.volume | 23 | - |
dc.identifier.issue | 26 | - |
dc.identifier.spage | 3884 | - |
dc.identifier.epage | 3898 | - |
dc.identifier.isi | WOS:000412330000011 | - |
dc.publisher.place | Netherlands | - |
dc.identifier.issnl | 1381-6128 | - |