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dc.contributor.authorNatticha Sumneangen_US
dc.contributor.authorNatthaphat Siri-Angkulen_US
dc.contributor.authorSirinart Kumfuen_US
dc.contributor.authorSiriporn C. Chattipakornen_US
dc.contributor.authorNipon Chattipakornen_US
dc.description.abstract© 2019 Elsevier Inc. Excessive iron accumulation in the heart can lead to iron overload cardiomyopathy (IOC), the leading cause of death in hemochromatosis patients. Current understanding regarding the mechanism by which iron overload causes a deterioration in cardiac performance, mitochondrial dysfunction, and impaired mitochondrial dynamics remains limited. Ferroptosis, a newly identified form of regulated cell death, has recently been revealed influencing the pathophysiological process of IOC. Nevertheless, the direct effect of cardiac iron overload on ferroptotic cell death is incompletely characterized. This review article comprehensively summarizes and discusses the effects of iron overload on cardiac mitochondrial function, cardiac mitochondrial dynamics, ferroptosis of cardiomyocytes, and left ventricular function in in vitro and in vivo reports. This review also provides relevant consistent and controversial information which can facilitate further mechanistic investigation into iron-induced cardiac dysfunction in the clinical setting in the near future.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleThe effects of iron overload on mitochondrial function, mitochondrial dynamics, and ferroptosis in cardiomyocytesen_US
article.title.sourcetitleArchives of Biochemistry and Biophysicsen_US
article.volume680en_US Mai Universityen_US
Appears in Collections:CMUL: Journal Articles

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