| Literature DB >> 29874997 |
Motoi Kobayashi1, Tomohiro Suhara1,2, Yuichi Baba1,3, Nicholas K Kawasaki1, Jason K Higa1, Takashi Matsui1.
Abstract
Iron is an essential mineral required for a variety of vital biological functions. Despite being vital for life, iron also has potentially toxic aspects. Iron has been investigated as a risk factor for coronary artery disease (CAD), however, iron's toxicity in CAD patients still remains controversial. One possible mechanism behind the toxicity of iron is "ferroptosis", a newly described form of irondependent cell death. Ferroptosis is an iron-dependent form of regulated cell death that is distinct from apoptosis, necroptosis, and other types of cell death. Ferroptosis has been reported in ischemiareperfusion (I/R) injury and several other diseases. Recently, we reported that ferroptosis is a significant form of cell death in cardiomyocytes. Moreover, myocardial hemorrhage, a major event in the pathogenesis of heart failure, could trigger the release of free iron into cardiac muscle and is an independent predictor of adverse left ventricular remodeling after myocardial infarction. Iron deposition in the heart can now be detected with advanced imaging methods, such as T2 star (T2*) cardiac magnetic resonance imaging, which can non-invasively predict iron levels in the myocardium and detect myocardial hemorrhage, thus existing technology could be used to assess myocardial iron. We will discuss the role of iron in cardiovascular diseases and especially with regard to myocardial I/R injury. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.Entities:
Keywords: Myocardial infarction; ferroptosis; iron; ischemia-reperfusion injury; reactive oxygen species.
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Year: 2018 PMID: 29874997 PMCID: PMC6469984 DOI: 10.2174/1389450119666180605112235
Source DB: PubMed Journal: Curr Drug Targets ISSN: 1389-4501 Impact factor: 3.465