{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,28]],"date-time":"2025-05-28T12:49:04Z","timestamp":1748436544715},"reference-count":7,"publisher":"American Scientific Publishers","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["j nanosci nanotechnol"],"published-print":{"date-parts":[[2021,2,1]]},"abstract":"<jats:p>The myocardial I\/R damage is very complicated. Apoptosis is considered to its a critical mechanism. During the cardiac muscle I\/R process, oxygen-free radicals play a pivotal role. Arrhythmias, as well as enlargement of the area of myocardial infarction after cardiac muscle I\/R process,\n are caused by adequate blast generated O<jats:sup>2-<\/jats:sup> ion free radicals. During the ischemia-reperfusion process, a large amount of O<jats:sup>2-<\/jats:sup> ion free radicals destroyed the cell structure, and it undergoes lipid peroxidation with unsaturated fatty acids that contain a large number of\n phospholipids in the cell membrane, causing membrane proteins such as ion channels and enzymes on the cell membrane. The activity of cell is reduced, which affects the function of cell membrane and organelle membrane, destroys its integrity and reduces fluidity.We observed the effects of cerium\n dioxide nanoparticles on glutathione peroxidase as well as superoxide dismutase, also propionate in myocardial tissue of I\/R injury in the mouse. Its effects of malondialdehyde and apoptosis were explored to see its protective effect and to provide more preventive measures for ischemia-reperfusion\n injury.<\/jats:p>","DOI":"10.1166\/jnn.2021.18643","type":"journal-article","created":{"date-parts":[[2020,11,13]],"date-time":"2020-11-13T04:53:47Z","timestamp":1605243227000},"page":"1397-1402","source":"Crossref","is-referenced-by-count":6,"title":["Effect of Composite Nanoparticle CeO<sub>2<\/sub> on Myocardial Ischemic Re-Infusion of Cardio Myocyte Apoptosis in Mouse"],"prefix":"10.1166","volume":"21","author":[{"given":"Chengbin","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Beijing Anzhen Hospital Capital Medical University, Beijing, 100029, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Peking University International Hospital, Beijing, 102206, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiamei","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Beijing Anzhen Hospital Capital Medical University, Beijing, 100029, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Beibei","family":"Cao","sequence":"additional","affiliation":[{"name":"Ambery Biotechnologies, Beijing, 102609, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mingwei","family":"He","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Beijing Anzhen Hospital Capital Medical University, Beijing, 100029, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"17","reference":[{"issue":"(2)","key":"r1","doi-asserted-by":"crossref","first-page":"pp.257","DOI":"10.1016\/j.yexcr.2018.04.004","article-title":"Regulation of VDAC1 contributes to the cardio-protective effects of penehyclidine hydrochloride during myocar-dial ischemia\/reperfusion.","volume":"367","author":"Lin","year":"2018","journal-title":"Experimental Cell Research"},{"issue":"(7)","key":"r2","doi-asserted-by":"crossref","first-page":"pp.2672","DOI":"10.1073\/pnas.1821022116","article-title":"Ferroptosis as a Target for Protection Against Cardiomyopathy.","volume":"116","author":"Fang","year":"2019","journal-title":"Proceedings of the National Academy of Sciences"},{"issue":"(3)","key":"r3","first-page":"pp.93","article-title":"Critical role of mitochondrial ROS is dependent on their site of production on the electron transport chain in ischemic heart.","volume":"6","author":"Madungwe","year":"2016","journal-title":"American Journal of Cardiovascular Disease"},{"issue":"(2)","key":"r4","doi-asserted-by":"crossref","first-page":"pp.354","DOI":"10.1016\/j.molcel.2018.10.042","article-title":"Role of mitochondria in ferroptosis.","volume":"73","author":"Gao","year":"2019","journal-title":"Molecular Cell"},{"issue":"(4)","key":"r5","doi-asserted-by":"crossref","first-page":"pp.1900","DOI":"10.1152\/ajpheart.01244.2003","article-title":"Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload.","volume":"288","author":"Sun","year":"2005","journal-title":"AJP Heart & Circulatory Physiology"},{"issue":"(3)","key":"r6","doi-asserted-by":"crossref","first-page":"pp.478","DOI":"10.1093\/cvr\/cvp421","article-title":"Cardioprotec-tion by GSK-3 inhibition: Role of enhanced glycogen synthesis and attenuation of calcium overload.","volume":"86","author":"Omar","year":"2010","journal-title":"Cardiovascular Research"},{"issue":"(2)","key":"r7","doi-asserted-by":"crossref","first-page":"pp.838","DOI":"10.1016\/j.bbrc.2016.08.034","article-title":"CISD1 inhibits ferroptosis by protection against mito-chondrial lipid peroxidation.","volume":"478","author":"Yuan","year":"2016","journal-title":"Biochemical and Biophysical Research Communications"}],"container-title":["Journal of Nanoscience and Nanotechnology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ingentaconnect.com\/content\/asp\/jnn\/2021\/00000021\/00000002\/art00081","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,12,24]],"date-time":"2020-12-24T04:52:28Z","timestamp":1608785548000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ingentaconnect.com\/content\/10.1166\/jnn.2021.18643"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,2,1]]},"references-count":7,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2021,2,1]]}},"alternative-id":["1533-4880(20210201)21:2L.1397;1-"],"URL":"https:\/\/doi.org\/10.1166\/jnn.2021.18643","relation":{},"ISSN":["1533-4880"],"issn-type":[{"value":"1533-4880","type":"print"}],"subject":[],"published":{"date-parts":[[2021,2,1]]}}}