Keshan disease: An endemic cardiomyopathy in China
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Cited by (104)
PPAR-γ with its anti-fibrotic action could serve as an effective therapeutic target in T-2 toxin-induced cardiac fibrosis of rats
2021, Food and Chemical ToxicologyCitation Excerpt :Food contaminated with T-2 toxin is purportedly a predisposing factor in the aetiology of Keshan disease (KSD) (Lei et al., 2016; Yang et al., 1993), which is an endemic cardiomyopathy particularly affecting children and young women in China with the character of multifocal necrosis and replacement fibrosis of the myocardium, leading to acute or chronic heart failure (Li et al., 1985; Sun, 2010; Wei et al., 2011). Clinical and experimental studies have shown that KSD is caused by a variety of factors, among which selenium deficiency and viral infection are important, but some mycotoxins, such as T-2 toxin, produced by grain contaminated with fungi may also cause poisoning (Ferreras et al., 2013; Li et al., 1985; Yang et al., 2020). To date, several studies have examined the close relationship of T-2 toxin with cardiomyocyte injury.
Selenium
2020, Present Knowledge in Nutrition: Basic Nutrition and MetabolismConsequences of mutations and inborn errors of selenoprotein biosynthesis and functions
2018, Free Radical Biology and MedicineCitation Excerpt :In this review, we will revise different human diseases linked to inborn errors in selenoprotein biosynthesis factors and to individual selenoproteins. Keshan disease, a dilated cardiomyopathy, first described in Chinese medical literature [18], was the first human disease linked to selenium deficiency. Posteriorly, Kashin-Beck disease and myxedematous endemic cretinism were also related to selenium deficiency [1], the same as two cases of intractable childhood epilepsy [19].
Interplay between autophagy and apoptosis in selenium deficient cardiomyocytes in chicken
2017, Journal of Inorganic BiochemistrySelenium deficiency associated porcine and human cardiomyopathies
2015, Journal of Trace Elements in Medicine and Biology
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Received from the Institute of Endemic Disease, Norman Bethune University of Medical Sciences, Changchun, Jilin, The People's Republic of China.