Do reactive oxygen species damage or protect the heart in ischemia and reperfusion? Analysis on experimental and clinical data
The role of reactive oxygen species (ROS) in ischemic and reperfusion (I/R) injury of the heart has been discussed for more than 40 years. It has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated heart. Antioxidants were found to have the abil...
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Veröffentlicht in: | Journal of biomedical research 2023-07, Vol.37 (4), p.268-280 |
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container_title | Journal of biomedical research |
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creator | Maslov, Leonid N Naryzhnaya, Natalia V Sirotina, Maria Mukhomedzyanov, Alexandr V Kurbatov, Boris K Boshchenko, Alla A Ma, Huijie Zhang, Yi Fu, Feng Pei, Jianming Azev, Viacheslav N Pereverzev, Vladimir A |
description | The role of reactive oxygen species (ROS) in ischemic and reperfusion (I/R) injury of the heart has been discussed for more than 40 years. It has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated heart. Antioxidants were found to have the ability to mitigate I/R injury of the heart. However, it is unclear whether their cardioprotective effect truly depends on the decrease of ROS levels in myocardial tissues. Since high doses and high concentrations of antioxidants were experimentally used, it is highly likely that the cardioprotective effect of antioxidants depends on their interaction not only with free radicals but also with other molecules. It has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic preconditioning. Consequently, there is evidence that ROS protect the heart against the I/R injury. |
doi_str_mv | 10.7555/JBR.36.20220261 |
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Antioxidants were found to have the ability to mitigate I/R injury of the heart. However, it is unclear whether their cardioprotective effect truly depends on the decrease of ROS levels in myocardial tissues. Since high doses and high concentrations of antioxidants were experimentally used, it is highly likely that the cardioprotective effect of antioxidants depends on their interaction not only with free radicals but also with other molecules. It has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic preconditioning. 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It has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic preconditioning. 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Analysis on experimental and clinical data</atitle><jtitle>Journal of biomedical research</jtitle><addtitle>J Biomed Res</addtitle><date>2023-07-28</date><risdate>2023</risdate><volume>37</volume><issue>4</issue><spage>268</spage><epage>280</epage><pages>268-280</pages><issn>1674-8301</issn><eissn>2352-4685</eissn><abstract>The role of reactive oxygen species (ROS) in ischemic and reperfusion (I/R) injury of the heart has been discussed for more than 40 years. It has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated heart. Antioxidants were found to have the ability to mitigate I/R injury of the heart. However, it is unclear whether their cardioprotective effect truly depends on the decrease of ROS levels in myocardial tissues. Since high doses and high concentrations of antioxidants were experimentally used, it is highly likely that the cardioprotective effect of antioxidants depends on their interaction not only with free radicals but also with other molecules. It has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic preconditioning. Consequently, there is evidence that ROS protect the heart against the I/R injury.</abstract><cop>China</cop><pub>Editorial Department of Journal of Biomedical Research</pub><pmid>37503710</pmid><doi>10.7555/JBR.36.20220261</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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title | Do reactive oxygen species damage or protect the heart in ischemia and reperfusion? Analysis on experimental and clinical data |
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